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Journal articles on the topic 'Chemical Induced Toxicity'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Fariss, Marc W., Marda K. Brown, John A. Schmitz, and Donald J. Reed. "Mechanism of chemical-induced toxicity." Toxicology and Applied Pharmacology 79, no. 2 (1985): 283–95. http://dx.doi.org/10.1016/0041-008x(85)90350-3.

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Fariss, Marc W., and Donald J. Reed. "Mechanism of chemical-induced toxicity." Toxicology and Applied Pharmacology 79, no. 2 (1985): 296–306. http://dx.doi.org/10.1016/0041-008x(85)90351-5.

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Souza Monteiro de Araújo, Daniel, Rafael Brito, Danniel Pereira-Figueiredo, et al. "Retinal Toxicity Induced by Chemical Agents." International Journal of Molecular Sciences 23, no. 15 (2022): 8182. http://dx.doi.org/10.3390/ijms23158182.

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Vision is an important sense for humans, and visual impairment/blindness has a huge impact in daily life. The retina is a nervous tissue that is essential for visual processing since it possesses light sensors (photoreceptors) and performs a pre-processing of visual information. Thus, retinal cell dysfunction or degeneration affects visual ability and several general aspects of the day-to-day of a person’s lives. The retina has a blood–retinal barrier, which protects the tissue from a wide range of molecules or microorganisms. However, several agents, coming from systemic pathways, reach the r

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Martin, WJ. "Pulmonary toxicity induced by chemical agents." European Respiratory Journal 3, no. 3 (1990): 375–76. http://dx.doi.org/10.1183/09031936.93.03030375.

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Kennedy, Katherine A., William N. Hait, and John S. Lazo. "Chemical modulation of bleomycin induced toxicity." International Journal of Radiation Oncology*Biology*Physics 12, no. 8 (1986): 1367–70. http://dx.doi.org/10.1016/0360-3016(86)90173-2.

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Colby, H. D. "Adrenal Gland Toxicity: Chemically Induced Dysfunction." Journal of the American College of Toxicology 7, no. 1 (1988): 45–69. http://dx.doi.org/10.3109/10915818809078702.

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Among the endocrine organs, the adrenal cortex appears to be the most vulnerable to chemically induced injury. A wide variety of chemicals has been found to cause morphological or functional lesions in the gland. Some of the lesions are highly localized to specific anatomical zones of the adrenal cortex, and the resulting functional deficits depend on the physiological role(s) of the zone affected. In addition, metabolic activation is an important factor contributing to the gland's vulnerability to chemical injury. For example, carbon tetrachloride (CCl4) causes adrenocortical necrosis, but on

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Rokad, Dharmin, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, and Anumantha G. Kanthasamy. "Exosomes as Mediators of Chemical-Induced Toxicity." Current Environmental Health Reports 6, no. 3 (2019): 73–79. http://dx.doi.org/10.1007/s40572-019-00233-9.

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Jaganathan, Keerthana, Mobeen Ur Rehman, Hilal Tayara, and Kil To Chong. "XML-CIMT: Explainable Machine Learning (XML) Model for Predicting Chemical-Induced Mitochondrial Toxicity." International Journal of Molecular Sciences 23, no. 24 (2022): 15655. http://dx.doi.org/10.3390/ijms232415655.

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Organ toxicity caused by chemicals is a serious problem in the creation and usage of chemicals such as medications, insecticides, chemical products, and cosmetics. In recent decades, the initiation and development of chemical-induced organ damage have been related to mitochondrial dysfunction, among several adverse effects. Recently, many drugs, for example, troglitazone, have been removed from the marketplace because of significant mitochondrial toxicity. As a result, it is an urgent requirement to develop in silico models that can reliably anticipate chemical-induced mitochondrial toxicity.

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Batt, A. M., and L. Ferrari. "Manifestations of chemically induced liver damage." Clinical Chemistry 41, no. 12 (1995): 1882–87. http://dx.doi.org/10.1093/clinchem/41.12.1882.

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Abstract Possible liver damage induced by chemicals or drugs must be detected early during drug development or industrial exposure, although damage is still difficult to predict, especially when immunotoxicity is involved. Liver toxicity may result from cytolysis, steatosis, cholestasis, phospholipidosis, or vascular lesions, most the outcome of a disadvantageous balance between chemicals or metabolites vs protective mechanisms, resulting from chemical dosage, genetic factors, or the immunoallergic status of the patient. Drug metabolism, lipid peroxidation, and thiol oxidation are frequently i

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Stavrakeva, K., M. Popova, M. Esad, et al. "Drug-Induced Liver Toxicity." Acta Medica Bulgarica 51, no. 4 (2024): 77–85. http://dx.doi.org/10.2478/amb-2024-0083.

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Abstract The liver performs many vital functions such as regulating homeostasis, bile production, storage of vitamins, and more. Another important function of the liver is to neutralize toxic substances entering the body. Substances entering the human body can be eliminated unchanged, retained unchanged, or undergo chemical transformation. Drugs are one of the most important and common causes of hepatotoxicity. It can manifest in various forms, ranging from elevated serum levels of transaminases to acute liver failure. The mechanisms of drug-induced liver damage may include the formation of a

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Hoyer, P. B., and I. G. Sipes. "Assessment of Follicle Destruction in Chemical-Induced Ovarian Toxicity." Annual Review of Pharmacology and Toxicology 36, no. 1 (1996): 307–31. http://dx.doi.org/10.1146/annurev.pa.36.040196.001515.

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Smith, Brian R., and William R. Brian. "The Role of Metabolism in Chemical-Induced Pulmonary Toxicity." Toxicologic Pathology 19, no. 4_part_1 (1991): 470–81. http://dx.doi.org/10.1177/0192623391019004-115.

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The lung is a target organ for the toxic effects of several chemical agents, including natural products, industrial chemicals, pesticides, environmental agents, and occasionally, drugs. Factors that establish the lung as a target organ include selective tissue exposure, high tissue oxygenation, and the presence of bioactivating systems that can generate toxic products from initially innocuous substances. Selective pulmonary exposure most often results from the fact that the lung serves as the major portal of entry for most airborne substances, but in some cases, selective exposure is the conse

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Meyer, Joel N., and Sherine S. L. Chan. "Sources, mechanisms, and consequences of chemical-induced mitochondrial toxicity." Toxicology 391 (November 2017): 2–4. http://dx.doi.org/10.1016/j.tox.2017.06.002.

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Hallinger, Daniel R., Hayley B. Lindsay, Katie Paul Friedman, Danielle A. Suarez, and Steven O. Simmons. "Respirometric Screening and Characterization of Mitochondrial Toxicants Within the ToxCast Phase I and II Chemical Libraries." Toxicological Sciences 176, no. 1 (2020): 175–92. http://dx.doi.org/10.1093/toxsci/kfaa059.

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Abstract Mitochondrial toxicity drives several adverse health outcomes. Current high-throughput screening assays for chemically induced mitochondrial toxicity typically measure changes to mitochondrial structure and may not detect known mitochondrial toxicants. We adapted a respirometric screening assay (RSA) measuring mitochondrial function to screen ToxCast chemicals in HepG2 cells using a tiered testing strategy. Of 1042 chemicals initially screened at a singlemaximal concentration, 243 actives were identified and rescreened at 7 concentrations. Concentration-response data for 3 respiration

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Indhu, S., S. Kalaimani, Sabarigrivasan Harish, and Gogulakrishnan Ramalingam. "Role of Steroids in Paint Thinner Induced Chemical Pneumonitis." Journal of Association of Pulmonologist of Tamil Nadu 7, no. 3 (2024): 120–22. http://dx.doi.org/10.4103/japt.japt_10_24.

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Abstract Paint thinners are organic hydrocarbons that contain a mixture of chemicals such as acetone, toluene, and xylene. Thinner poisoning is most common in children due to accidental ingestion. Acute poisoning can lead to various systemic manifestations such as chemical pneumonitis, arrhythmia, dermatitis, and metabolic acidosis. Chronic toxicity leads to encephalopathy and weakness. Usually, management of chemical pneumonitis following hydrocarbon aspiration is symptomatic and the role of steroids is controversial. We report the case of a 47-year-old female who presented with ingestion of

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Koontz, Jason M., Blair C. R. Dancy, Cassandra L. Horton, Jonathan D. Stallings, Valerie T. DiVito, and John A. Lewis. "The Role of the Human Microbiome in Chemical Toxicity." International Journal of Toxicology 38, no. 4 (2019): 251–64. http://dx.doi.org/10.1177/1091581819849833.

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There is overwhelming evidence that the microbiome must be considered when evaluating the toxicity of chemicals. Disruption of the normal microbial flora is a known effect of toxic exposure, and these disruptions may lead to human health effects. In addition, the biotransformation of numerous compounds has been shown to be dependent on microbial enzymes, with the potential for different host health outcomes resulting from variations in the microbiome. Evidence suggests that such metabolism of environmental chemicals by enzymes from the host's microbiota can affect the toxicity of that chemical

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Pant, Satish C., and Vinay Lomash. "Sulphur Mustard Induced Toxicity, Mechanism of Action and Current Medical Management." Defence Life Science Journal 1, no. 1 (2016): 07. http://dx.doi.org/10.14429/dlsj.1.10089.

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<p>Sulphur mustard (SM), chemically, bis (2-chloroethyl) sulphide is a bifunctional alkylating agent that causes cutaneous blisters in human or animals. It was first used in the World War I. Since then, there have been 11 conflicts where SM allegedely had caused mass distruction. Additionally, discarded weapons and stockpiles periodically come to surface during agricultural or fishing activities leading to serious injury. Concerns for threat to modern societies by the serious effects of SM, agreements to ban its production and the use has been made as per 1993 chemical weapons convention

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Rembovskiy, V. R., and L. A. Mogilenkova. "Personalized toxicology: phenomenology, relevance, development prospects." Medical academic journal 20, no. 3 (2020): 61–73. http://dx.doi.org/10.17816/maj34959.

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Personalized toxicology is a research area that studies the individual toxicity of hazardous chemical compounds by experimental and clinical toxicology based on new molecular medicine approaches, including genetics and epigenomics, for prevention, diagnosis, and treatment of chemically induced diseases. Goal of Research.To study individual genetically and epigenetically induced mechanisms of bodys response to exposure to chemical substances, and their effect on preclinical and reversible changes, development of intoxications, and long-term effects, as well as assessment of the individual

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Liu, Ruifeng, Xueping Yu, and Anders Wallqvist. "Using Chemical-Induced Gene Expression in Cultured Human Cells to Predict Chemical Toxicity." Chemical Research in Toxicology 29, no. 11 (2016): 1883–93. http://dx.doi.org/10.1021/acs.chemrestox.6b00287.

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Singh, Harpal, Elissa Purnell, and Carion Smith. "Mechanistic Study on Aniline-Induced Erythrocyte Toxicity." Archives of Industrial Hygiene and Toxicology 58, no. 3 (2007): 275–85. http://dx.doi.org/10.2478/v10004-007-0018-2.

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Mechanistic Study on Aniline-Induced Erythrocyte ToxicityStrategies for the use of bio-indicators in the prediction of environmental damage should include mechanistic research. This study involves the relationship between the chemical structure and hemotoxic markers of aniline and its halogenated analogs. Aniline-induced methemoglobinemia, loss of circulating blood cells, blood stability, glutathione depletion and membrane cytoskeletal changes were assessed following exposure to phenylhydroxylamine (PHA), para-fluoro-, para-bromo-, and para-iodo in male Sprague-Dawley rats. Methemoglobin was d

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Tegg, Robert S., Ross Corkrey, and Calum R. Wilson. "Relationship Between the Application of Foliar Chemicals to Reduce Common Scab Disease of Potato and Correlation with Thaxtomin A Toxicity." Plant Disease 96, no. 1 (2012): 97–103. http://dx.doi.org/10.1094/pdis-05-11-0397.

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Production of the phytotoxin thaxtomin A by pathogenic Streptomyces spp. is essential for induction of common scab disease in potato. The disease can be significantly reduced by a range of chemicals applied as foliar sprays before tuber initiation. We tested a range of chemicals that had previously demonstrated varying capacities to reduce common scab for both disease suppression and their ability to inhibit thaxtomin A toxicity in both ‘Desiree’ and ‘Russet Burbank’ potato. Our results for disease suppression generally supported previous studies. Our tuber slice assays with thaxtomin A showed

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Smith, B. R., and W. R. Brian. "The Role of Metabolism in Chemical-Induced Pulmonary Toxicity*1." Toxicologic Pathology 19, no. 4-1 (1991): 470–81. http://dx.doi.org/10.1177/019262339101900415.

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Ramaiah, Shashi K., Udayan Apte, and Harihara M. Mehendale. "Diet Restriction as a Protective Mechanism in Noncancer Toxicity Outcomes: A Review." International Journal of Toxicology 19, no. 6 (2000): 413–24. http://dx.doi.org/10.1080/109158100750058776.

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It is well documented that diet restriction (DR) increases life expectancy, slows aging, and decreases the incidence of a variety of age-associated diseases including cancer and chemical-induced carcinogenesis. With regard to chemical toxicity, very few studies have attempted to investigate the effects of DR on noncancer toxicity outcomes. This review summarizes the findings of how DR influences acute toxicity outcomes and mechanisms. DR-induced protection in ozone lung inflammation, acute toxicity of isoproterenol, ganciclovir-, aspirin-and acidified ethanol-induced gastric injury are discuss

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Smith, Wanli W., Darrell D. Norton, Myriam Gorospe та ін. "Phosphorylation of p66Shc and forkhead proteins mediates Aβ toxicity". Journal of Cell Biology 169, № 2 (2005): 331–39. http://dx.doi.org/10.1083/jcb.200410041.

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Excessive accumulation of amyloid β-peptide (Aβ) plays an early and critical role in synapse and neuronal loss in Alzheimer's Disease (AD). Increased oxidative stress is one of the mechanisms whereby Aβ induces neuronal death. Given the lessened susceptibility to oxidative stress exhibited by mice lacking p66Shc, we investigated the role of p66Shc in Aβ toxicity. Treatment of cells and primary neuronal cultures with Aβ caused apoptotic death and induced p66Shc phosphorylation at Ser36. Ectopic expression of a dominant-negative SEK1 mutant or chemical JNK inhibition reduced Aβ-induced JNK activ

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Morris, Johnathan, Elizabeth J. Bealer, Ivan D. S. Souza, et al. "Chemical Exposure-Induced Developmental Neurotoxicity in Head-Regenerating Schmidtea mediterranea." Toxicological Sciences 185, no. 2 (2021): 220–31. http://dx.doi.org/10.1093/toxsci/kfab132.

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Abstract The growing number of commercially used chemicals that are under-evaluated for developmental neurotoxicity (DNT) combined with the difficulty in describing the etiology of exposure-related neurodevelopmental toxicity has created a reticent threat to human health. Current means of screening chemicals for DNT are limited to expensive, time-consuming, and labor-intensive traditional laboratory animal models. In this study, we hypothesize that exposed head-regenerating planarian flatworms can effectively and efficiently categorize DNT in known developmental neurotoxins (ethanol and bisphe

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den Besten, C., A. Brouwer, I. M. C. M. Rietjens, and P. J. van Bladeren. "Biotransfiormation and Toxicity of Halogenated Benzenes." Human & Experimental Toxicology 13, no. 12 (1994): 866–75. http://dx.doi.org/10.1177/096032719401301209.

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1 Multiple potentially harmful metabolites can be distinguished in the metabolic activation of halogenated benzenes: epoxides, phenols, benzoquinones and benzoquinone-derived glutathione conjugates. 2 The role of these (re-) active metabolites in the toxic effects induced by halogenated benzenes such as hepatotoxicity, nephrotoxicity, porphyria and thyroid toxicity is discussed. 3 Evidence is presented suggesting that the formation of reactive benzoquinone metabolites rather than the traditional epoxides is linked to halogenated benzene-induced hepatotoxicity. 4 A crucial role for the benzoqui

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Trosko, James E. "Commentary on ‘‘Toxicity Testing in the 21st Century: A vision and a Strategy’’: Stem Cells and Cell-Cell Communication as Fundamental Targets in Assessing the Potential Toxicity of Chemicals." Human & Experimental Toxicology 29, no. 1 (2010): 21–29. http://dx.doi.org/10.1177/0960327109354663.

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Faced with the reality of our current methods of drug discovery and toxicity assessment of all chemicals is less than perfect, the Report, ‘‘Toxicity Testing in the 21 st Century: A Vision and a Strategy’’, posed a reality check on all scientific efforts to find new conceptual and technical approaches for being better predictors of potential human health effects. This Commentary is a challenge to both the current paradigms and techniques to test chemicals for their potential toxicities. While, clearly, our scientific understanding of the mechanisms of chemical-induced toxicity and of the patho

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Paul, Tanushree, Sumitava Roy, Raktim Mukherjee, Saikat Pramanik, and Susanta Roy Karmakar. "Assessment of toxicity of formalin use as food preservative evidenced by cytotoxic and genotoxic effects in mice: An in vivo study." INTERNATIONAL JOURNAL OF EXPERIMENTAL RESEARCH AND REVIEW 12 (August 30, 2017): 43–49. http://dx.doi.org/10.52756/ijerr.2017.v12.006.

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The present study was conducted to find out the deleterious effects of formalin by studying cytogenetical parameters, namely chromosome aberration (CA), mitotic indices (MI) and sperm head anomaly (SHA) in mice. Healthy mice weighing between 20-25 gms were fed with formalin at a dose 0.042mg/kg body weight to find out whether there is any toxicity induced by this chemical. Experiments were carried out at three different fixation intervals, namely 7 Days (7D), 14 Days (14D) and 21 Days (21D), maintaining suitable controls. The investigation reveals that feeding of formalin induced geno-toxicity

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Hartman, Jessica, Latasha Smith, Kacy Gordon, et al. "Chemical-induced toxicity is ameliorated by swimming exercise in caenorhabditis elegans." Drug Metabolism and Pharmacokinetics 34, no. 1 (2019): S30. http://dx.doi.org/10.1016/j.dmpk.2018.09.117.

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Liu, Xiaoyi, Lihong Fan, Chengrong Lu, Shutao Yin, and Hongbo Hu. "Functional Role of p53 in the Regulation of Chemical-Induced Oxidative Stress." Oxidative Medicine and Cellular Longevity 2020 (February 29, 2020): 1–10. http://dx.doi.org/10.1155/2020/6039769.

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The nuclear transcription factor p53, discovered in 1979, has a broad range of biological functions, primarily the regulation of apoptosis, the cell cycle, and DNA repair. In addition to these canonical functions, a growing body of evidence suggests that p53 plays an important role in regulating intracellular redox homeostasis through transcriptional and nontranscriptional mechanisms. Oxidative stress induction and p53 activation are common responses to chemical exposure and are suggested to play critical roles in chemical-induced toxicity. The activation of p53 can exert either prooxidant or

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Mrunali, Dhakare* Dr. Gopal Bihani Dr. Pavan N. Folane Dr. Kailash Biyani. "Evaluation Of In-Vivo Hepato-Protective Activity of Polyherbal Extract Against Chemically Induced-Hepatotoxic Rats." International Journal of Pharmaceutical Sciences 3, no. 5 (2025): 3823–35. https://doi.org/10.5281/zenodo.15490469.

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Chemically induced hepatotoxicity in rats, also known as drug-induced liver injury (DILI), is a widely used model for studying liver damage caused by various chemicals and drugs. Researchers use this model to understand the mechanisms of hepatotoxicity, develop new therapies, and assess the safety of new drugs before they are tested in humans. Commonly used hepatotoxins in rats include Carbon Tetrachloride (CCl4), Thioacetamide (TAA), Paracetamol (Acetaminophen), D-Galactosamine, and Dimethyl nitrosamine (DMN). Histopathological and biochemical parameters are assessed through examination of li

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Garric, J., B. Vollat, D. K. Nguyen, M. Bray, B. Migeon, and A. Kosmala. "Ecotoxicological and chemical characterization of municipal wastewater treatment plant effluents." Water Science and Technology 33, no. 6 (1996): 83–91. http://dx.doi.org/10.2166/wst.1996.0084.

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The toxicity and the chemical quality of three municipal wastewater effluents have been studied. Acute and sub-chronic bioassays were carried out. We also measured the induction of the hepatic ethoxy resorufin-O-deethylase enzymatic activity (EROD) of fish exposed to the effluents. Chemical analysis allowed to identify the most frequent substances detected in the effluents. From chemical data and results of bioassays we conclude that ammonia concentration explains a part of the lethal toxicity. But chronic toxicity tests carried out with whole effluents or extracted chemical fractions showed t

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Maleeff, Beverly E., Tracy L. Gales, Padma K. Narayanan, Mark A. Tirmenstein, and Timothy K. Hart. "Microscopic Analysis of Oxidative Stress in Cultured Cells. I. Confocal Microscopy." Microscopy and Microanalysis 7, S2 (2001): 634–35. http://dx.doi.org/10.1017/s143192760002924x.

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Cellular oxidative stress, a common mechanism of drug-induced toxicity, is a result of the formation of reactive oxygen species (ROS) in response to chemical stimuli. An endpoint of ROS production is lipid peroxidation, which can in turn lead to disruption of cellular membranes, loss of mitochondrial function, protein oxidation and DNA damage. This toxicity can be organ-specific due to the varying capacities of tissues to handle oxidative events. Liver is particularly sensitive to the effects of oxidative stress, and hepatic toxicity is seen clinically. HepG2 cells are an immortalized human he

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Ibrahim Ali, Haneen, Baydaa Hussain Mutlak, Sohad Abdulkaleg Alshareef, and Zamzam Alhuwaymil. "Effect of CCl4 on Renal Tissues of Male Mice and Prevented by Pretreatment with Bromelain Loaded with Gold Nanoparticles: Histopathological and Caspase-9 Expression Alterations." Trends in Sciences 21, no. 12 (2024): 8358. http://dx.doi.org/10.48048/tis.2024.8358.

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The study aimed to investigate the potential protective effect of bromelain on renal histopathological changes induced by carbon tetrachloride (CCl4) in albino mice. CCl4 is widely used in the chemical industry but is also known to cause toxicity to various organs including the brain, liver, kidneys and lungs. In this study, 49 animals were divided into 7 equal groups. The kidneys of the mice were examined to assess histopathological changes and immunohistochemical markers, specifically caspase-9. The groups that received bromelain solution coated with gold nanoparticles demonstrated greater p

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Lupu, Diana, Patrik Andersson, Carl-Gustaf Bornehag, et al. "The ENDpoiNTs Project: Novel Testing Strategies for Endocrine Disruptors Linked to Developmental Neurotoxicity." International Journal of Molecular Sciences 21, no. 11 (2020): 3978. http://dx.doi.org/10.3390/ijms21113978.

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Ubiquitous exposure to endocrine-disrupting chemicals (EDCs) has caused serious concerns about the ability of these chemicals to affect neurodevelopment, among others. Since endocrine disruption (ED)-induced developmental neurotoxicity (DNT) is hardly covered by the chemical testing tools that are currently in regulatory use, the Horizon 2020 research and innovation action ENDpoiNTs has been launched to fill the scientific and methodological gaps related to the assessment of this type of chemical toxicity. The ENDpoiNTs project will generate new knowledge about ED-induced DNT and aims to devel

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Joyce, Trujillo, Osorio-Chavéz Fanny, Medina-Campos Omar Noel, Loredo María Lilia, Pedraza-Chaverri Jose, and Arriaga Sonia. "Curcumin Prevents Renal Dysfunction, Proteinaceous and Granular Cast Formation in Tubular Lumen in Kidney of Mice Exposed to Formaldehyde Inhalation." Current Topics in Nutraceutical Research 17, no. 3 (2019): 291–97. http://dx.doi.org/10.37290/ctnr2641-452x.17:291-297.

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Formaldehyde is a volatile chemical compound that is commonly used in the chemical industry. Formaldehyde inhalation exposure has been associated with cancer, respiratory diseases, digestive and neurological disorders. Oxidative stress is one of the potential mechanisms by which formaldehyde inhalation induces toxicity. Curcumin is a natural compound endowed with antioxidant properties and my thus prevent formaldehyde-induced toxicity. This study aimed to examine the effects of formaldehyde inhalation on renal function and kidney structure of mice; the potential protective effects of curcumin

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Ghosh, Sreya, Jonathan De Smedt, Tine Tricot, et al. "HiPSC-Derived Hepatocyte-like Cells Can Be Used as a Model for Transcriptomics-Based Study of Chemical Toxicity." Toxics 10, no. 1 (2021): 1. http://dx.doi.org/10.3390/toxics10010001.

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Traditional toxicity risk assessment approaches have until recently focussed mainly on histochemical readouts for cell death. Modern toxicology methods attempt to deduce a mechanistic understanding of pathways involved in the development of toxicity, by using transcriptomics and other big data-driven methods such as high-content screening. Here, we used a recently described optimised method to differentiate human induced pluripotent stem cells (hiPSCs) to hepatocyte-like cells (HLCs), to assess their potential to classify hepatotoxic and non-hepatotoxic chemicals and their use in mechanistic t

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Brossman, Kelly H., Bradley E. Carlson, Amber N. Stokes, and Tracy Langkilde. "Eastern Newt (Notophthalmus viridescens) larvae alter morphological but not chemical defenses in response to predator cues." Canadian Journal of Zoology 92, no. 4 (2014): 279–83. http://dx.doi.org/10.1139/cjz-2013-0244.

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Prey traits are often modified in response to exposure to predators, a phenomenon known as predator-induced phenotypic plasticity. Morphological plasticity in response to predator cues is well documented in amphibians; however, predator-induced chemical defenses have received relatively little attention. The Eastern Newt (Notophthalmus viridescens (Rafinesque, 1820)), which possesses tetrodotoxin—a toxin for chemical defense, is most vulnerable to predation during its larval stage. We assessed whether exposing Eastern Newt larvae to predator scent cues (from dragonfly larvae) would elicit chan

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Knudsen, TB, B. Klieforth, and W. Slikker. "Programming microphysiological systems for children’s health protection." Experimental Biology and Medicine 242, no. 16 (2017): 1586–92. http://dx.doi.org/10.1177/1535370217717697.

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Microphysiological systems (MPS) and computer simulation models that recapitulate the underlying biology and toxicology of critical developmental transitions are emerging tools for developmental effects assessment of drugs/chemicals. Opportunities and challenges exist for their application to alternative, more public health relevant and efficient chemical toxicity testing methods. This is especially pertinent to children’s health research and the evaluation of complex embryological and reproductive impacts of drug/chemical exposure. Scaling these technologies to higher throughput is a key chal

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Pessoa, Renata Torres, Isabel Sousa Alcântara, Lucas Yure Santos da Silva, et al. "Ximenia americana L.: Chemical Characterization and Gastroprotective Effect." Analytica 4, no. 2 (2023): 141–58. http://dx.doi.org/10.3390/analytica4020012.

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Ximenia americana L., popularly known in Brazil as “ameixa do-mato, ameixa-brava, and ameixa-do-sertão,” is widely used in folk medicine to treat several intestinal disorders. The present study assessed the potential mechanisms of action underlying the gastroprotective activity of the hydroethanolic extract of Ximenia americana L. (EHXA) stem bark. The acute toxicity of EHXA was estimated, and later, the gastroprotective effect in mice was assessed through acute models of gastric lesions induced by acidified or absolute ethanol and indomethacin, where the following mechanisms were pharmacologi

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Steinritz, Dirk, Bernhard Stenger, Alexander Dietrich, Thomas Gudermann, and Tanja Popp. "TRPs in Tox: Involvement of Transient Receptor Potential-Channels in Chemical-Induced Organ Toxicity—A Structured Review." Cells 7, no. 8 (2018): 98. http://dx.doi.org/10.3390/cells7080098.

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Chemicals can exhibit significant toxic properties. While for most compounds, unspecific cell damaging processes are assumed, a plethora of chemicals exhibit characteristic odors, suggesting a more specific interaction with the human body. During the last few years, G-protein-coupled receptors and especially chemosensory ion channels of the transient receptor potential family (TRP channels) were identified as defined targets for several chemicals. In some cases, TRP channels were suggested as being causal for toxicity. Therefore, these channels have moved into the spotlight of toxicological re

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Saandeep, Kalavatala, Ajit Vikram, Durga Nand Tripathi, Poduri Ramarao, and Gopabandhu Jena. "Influence of Hyperglycaemia on Chemical-Induced Toxicity: Study with Cyclophosphamide in Rat." Basic & Clinical Pharmacology & Toxicology 105, no. 4 (2009): 236–42. http://dx.doi.org/10.1111/j.1742-7843.2009.00433.x.

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Zhu, Shishu, Shih-Hsin Ho, Chao Jin, Xiaoguang Duan, and Shaobin Wang. "Nanostructured manganese oxides: natural/artificial formation and their induced catalysis for wastewater remediation." Environmental Science: Nano 7, no. 2 (2020): 368–96. http://dx.doi.org/10.1039/c9en01250h.

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Melnick, Ronald L., and James Huff. "Liver Carcinogenesis is Not a Predicted Outcome of Chemically Induced Hepatocyte Proliferation." Toxicology and Industrial Health 9, no. 3 (1993): 415–38. http://dx.doi.org/10.1177/074823379300900303.

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Cell proliferation has long been recognized as a basic component of multistage carcinogenesis. Based largely on the finding that certain nongenoloxic chemical carcinogens induce cell proliferation in the same organ that develops tumors after long-term exposure, some suggest that the increased rates of cell division account for the carcinogenicity of these chemicals. This paper examines relationships between chemically induced liver toxicity, cell proliferation, and liver carcinogenesis; major factors include consistency, transient vs. sustained dose-response correspondence, and scientific plau

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Flohr, Letícia, Armando Borges de Castilhos Júnior, and William Gerson Matias. "Acute and Chronic Toxicity of Soluble Fractions of Industrial Solid Wastes onDaphnia magnaandVibrio fischeri." Scientific World Journal 2012 (2012): 1–10. http://dx.doi.org/10.1100/2012/643904.

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Industrial wastes may produce leachates that can contaminate the aquatic ecosystem. Toxicity testing in acute and chronic levels is essential to assess environmental risks from the soluble fractions of these wastes, since only chemical analysis may not be adequate to classify the hazard of an industrial waste. In this study, ten samples of solid wastes from textile, metal-mechanic, and pulp and paper industries were analyzed by acute and chronic toxicity tests withDaphnia magnaandVibrio fischeri. A metal-mechanic waste (sample MM3) induced the highest toxicity level toDaphnia magna(CE50,48 h=2

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Purish, L. M., D. R. Abdulina, and G. O. Iutynska. "Inhibitors of Corrosion Induced by Sulfate-Reducing Bacteria." Mikrobiolohichnyi Zhurnal 83, no. 6 (2021): 95–109. http://dx.doi.org/10.15407/microbiolj83.06.095.

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Currently, a lot of researcher’s attention is devoted to the problem of microbiologically influenced corrosion (MIC), since it causes huge damages to the economy, initiating the destruction of oil and gas pipelines and other underground constructions. To protect industrial materials from MIC effects an organic chemical inhibitors are massively used. However, the problem of their use is associated with toxicity, dangerous for the environment that caused the need for development the alternative methods of MIC repression. At the review, the data about different types of inhibitors-biocides usage

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Gauvin, David V., Joshua D. Yoder, Rachel L. Tapp, and Theodore J. Baird. "Small Compartment Toxicity." International Journal of Toxicology 36, no. 1 (2016): 8–20. http://dx.doi.org/10.1177/1091581816648905.

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Life experiences, industrial/environmental exposures, and administration of Food and Drug Administration (FDA)-approved drugs may have unintended but detrimental effects on peripheral and central auditory pathways. Most relevant to the readership of this journal is the role that drug treatments approved by the FDA as safe and effective appear to interact with 3 independent modes of toxicity within the small compartment of the ear. What may seem to be trivial drug-induced toxicity has the potential to change important measures of quality of life and functional capacity of mid- to late-life pati

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Khanehzar, Ali, Juan C. Fraire, Min Xi, et al. "Nanoparticle–cell interactions induced apoptosis: a case study with nanoconjugated epidermal growth factor." Nanoscale 10, no. 14 (2018): 6712–23. http://dx.doi.org/10.1039/c8nr01106k.

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Antunes, Kátia Avila, Débora da Silva Baldivia, Paola dos Santos da Rocha, et al. "Antiobesity Effects of Hydroethanolic Extract of Jacaranda decurrens Leaves." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/4353604.

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Obesity is a worldwide epidemic that reduces life expectancy; therefore, the search for new alternative and effective treatments is ongoing. The aim of the present investigation was to identify the chemical compounds in the hydroethanolic extract of leaves of Jacaranda decurrens subsp. symmetrifoliolata and to evaluate their toxicity and antiobesity effects. High-performance liquid chromatography was used to identify the chemical constituents, and acute toxicity was evaluated in rats treated with doses of 2 and 5 g·kg−1 body mass. The antiobesity effect was determined in rats with hypercaloric

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Zalzala, Munaf Hashim, and Victoria S. Kareem. "Safranal Effect against Cyclophosphamide-Induced Liver Injury." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 30, no. 2 (2021): 208–13. http://dx.doi.org/10.31351/vol30iss2pp208-213.

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The liver is the primary organ for drug metabolism, elimination, Cyclophosphamid is the classical alkylating agent nitrogen mustard, its metabolism into two cytotoxic metabolites, and increase reactive oxygen species that is make liver toxicity. Safranal as the most abundant chemical in saffron essential oil, it have anti-oxidant, anti-inflammatory, antiapoptic and free radical scavenger activity. The aim of study is to assess the protective effects of safranal on the cyclophosphamide-induce liver toxicity in rat model. This occur by using five different groups of rats; control group, treatmen

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