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Journal articles on the topic 'Fluorouracil – Toxicology'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Gintjee, Thomas J., Robert Goodnough, Kai Li, Adina Badea, Kara L. Lynch, Eddie Garcia, and Daniel Repplinger. "Real-time comprehensive toxicology testing in the clinical management of accidental pediatric capecitabine ingestion." Journal of Oncology Pharmacy Practice 26, no. 7 (February 23, 2020): 1759–61. http://dx.doi.org/10.1177/1078155220906266.

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Introduction Capecitabine is an orally bioavailable prodrug of the chemotherapeutic agent, fluorouracil. Fluorouracil is converted to several active metabolites that induce a cytotoxic effect. Capecitabine toxicity can be life-threatening with a delayed presentation from ingestion. An oral antidote, uridine triacetate, exists but requires the administration of 20 total doses over a course of five days. Case report In this report, we describe a case where timely coordination with a clinical toxicology laboratory was utilized to drive clinical decision making and management. Two children were brought to the emergency department shortly after suspected capecitabine ingestion. Management and outcome Patients were admitted to the hospital and started on uridine triacetate. Real-time comprehensive toxicology testing of the children’s blood was used to rule out capecitabine toxicity and prevent several unnecessary days of hospitalization and doses of antidote. Patients were discharged safely. Discussion Real-time comprehensive toxicology testing on a patient’s blood may be a valuable resource in ruling out or confirming toxic exposure in accidental pediatric ingestion of chemotherapeutic agents like capecitabine when performed in a timely manner.

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2

Deepa Suruli, Fathima Bushra Sheriff Mirza, Gloria Jemmi Christobel R, Amuthavalli Kottaiswamy, Shila Samuel, and Vijayaraghavan Radhakrishnan. "Naringin and 5-fluorouracil suppress inflammatory Cytokines in human skin cancer cell line." International Journal of Research in Pharmaceutical Sciences 12, no. 1 (January 13, 2021): 729–33. http://dx.doi.org/10.26452/ijrps.v12i1.4172.

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Naringin is a citrus flavonoid recently studied for anti-inflammatory activity in numerous cancer cells. In this study, the anti-inflammatory properties of naringin along with 5-fluorouracil in human skin cancer cell lines A375 was analyzed. A375 cells were treated with naringin, 5-fluorouracil alone, and combination. MTT assay and cell viability assays was demonstrated to detect the inhibitory effects of naringin or 5-fluorouracil on cell proliferation. mRNA expression of TNFα, IL-6, IL-1β, and NFκB were determined using quantitative RT-PCR. The effect of naringin and 5-fluorouracil combination significantly inhibited the growth and proliferation of the A375 cells in a concentration dependent manner with the IC50 values of naringin (24.75 μM) 5-fluorouracil (2.5 μM). The combination of naringin+5-fluorouracil on A375 cell lines at a concentration of half IC50 values (12µM+1 μM). Naringin and 5-fluorouracil combination also decreased the level of TNFα, IL-6, IL-1β, and NFκB mRNA in the A375 cell line. Naringin and 5-fluorouracil exerted anti-inflammatory effect through the suppression of NF-kB, IL-1β, TNFα, IL-6 in A375 cells. Taken together, our results suggested that treating A375 with naringin and 5-fluorouracil combination may have future applications in treating skin cancers through its anti-inflammatory effect.

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3

Ohuchida, A., T. Hara, A. Furukawa, S. Sato, M. Katoh, N. Ishihara, and T. Shibuya. "Mutagenicity of 5-fluorouracil and its metabolites." Mutation Research/Environmental Mutagenesis and Related Subjects 253, no. 3 (December 1991): 269–70. http://dx.doi.org/10.1016/0165-1161(91)90201-i.

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4

Tan, Biqin, Jing Wang, Mengting Zhao, Yan Hu, Jiajia Wang, Bo Yang, QiaoJun He, Xiao Chun Yang, and Qinjie Weng. "TCF7L2 activation is required for myelin regeneration in 5-FU-induced demyelinating mice." Toxicology Research 4, no. 6 (2015): 1597–603. http://dx.doi.org/10.1039/c5tx00110b.

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5

Naren, Gerile, Lu Wang, Xiaolei Zhang, Lijuan Cheng, Shuai Yang, Jiajie Yang, Jiaojiao Guo, and Buhe Nashun. "The reversible reproductive toxicity of 5-fluorouracil in mice." Reproductive Toxicology 101 (April 2021): 1–8. http://dx.doi.org/10.1016/j.reprotox.2021.02.002.

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6

Polyzos, A., N. Tsavaris, A. Giannopoulos, C. Bacoyiannis, V. Papadimas, N. Kalahanis, G. Karatzas, et al. "Biochemical modulation of fluorouracil: comparison of methotrexate, folinic acid, and fluorouracil versus folinic acid and fluorouracil in advanced colorectal cancer: a randomized trial." Cancer Chemotherapy and Pharmacology 38, no. 3 (June 1996): 292–97. http://dx.doi.org/10.1007/s002800050485.

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7

Kopjar, Nevenka, Ivan Milas, Verica Garaj-Vrhovac, and Marija Gamulin. "Cytogenetic outcomes of adjuvant chemotherapy in non-target cells of breast cancer patients." Human & Experimental Toxicology 26, no. 5 (May 2007): 391–99. http://dx.doi.org/10.1177/0960327106076812.

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Spontaneous and chemotherapy-induced sister chromatid exchanges (SCES) and lymphocyte proliferation rate index (PRI) in cultured peripheral lymphocytes were evaluated in 30 patients with diagnosed breast cancer before and after adjuvant chemotherapy and in 30 healthy women with no known familial history of breast cancer. Before chemotherapy, the breast cancer patients had a significantly increased background level of SCE, and lowered PRI as compared with the healthy women. Marked inter-individual variations were observed in both endpoints among the patients. Significantly elevated frequency of SCE and depressed PRI were recorded in blood samples collected after the first cycle of chemotherapy, with high inter-individual variations in the responses to the chemotherapy. FAC (5-fluorouracil, adriamycin and cyclophosphamide) protocol was the most genotoxic of the protocols studied, but also AC (adriamycin, cyclophosphamide) and CMF (cyclophosphamide, methotrexate and 5-fluorouracil) clearly increased SCE. All protocols significantly retarded lymphocyte proliferation in vitro. Our findings indicate that both SCE and PRI may serve as sensitive biomarkers for the routine detection of critical lesions produced by the administration of antineoplastic drugs in the clinical setting, as well as for possible screening of high-risk individuals among patients who have successfully completed chemotherapy. Human & Experimental Toxicology (2007) 26 , 391—399

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8

Hirata, Kohji, and Toshiharu Horie. "Changes in Intestinal Absorption of 5-Fluorouracil-Treated Rats." Pharmacology & Toxicology 85, no. 3 (September 1999): 33–36. http://dx.doi.org/10.1111/j.1600-0773.1999.tb01060.x.

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9

Werbrouck, Bart F., Walter J. Pauwels, and Jan L. De Bleecker. "A case of 5-fluorouracil-induced peripheral neuropathy." Clinical Toxicology 46, no. 3 (January 2008): 264–66. http://dx.doi.org/10.1080/15563650701438763.

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10

Takano, Fumihide, Tomoaki Tanaka, Jiro Aoi, Nobuo Yahagi, and Shinji Fushiya. "Protective effect of (+)-catechin against 5-fluorouracil-induced myelosuppression in mice." Toxicology 201, no. 1-3 (September 2004): 133–42. http://dx.doi.org/10.1016/j.tox.2004.04.009.

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11

Lynch, D. W., R. L. Schuler, D. G. Davis, and R. D. Hood. "Eye abnormality in drosophila melanogaster exposed to 5-fluorouracil during development." Reproductive Toxicology 6, no. 3 (January 1992): 263–65. http://dx.doi.org/10.1016/0890-6238(92)90182-s.

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12

Hrushesky, William J. M., Rostislav Vyzula, and Patricia A. Wood. "Fertility maintenance and 5-fluorouracil timing within the mammalian fertility cycle." Reproductive Toxicology 13, no. 5 (September 1999): 413–20. http://dx.doi.org/10.1016/s0890-6238(99)00037-4.

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13

Tsibiribi, P., C. Bui-Xuan, B. Bui-Xuan, C. Lombard-Bohas, S. Duperret, M. Belkhiria, A. Tabib, G. Maujean, J. Descotes, and Q. Timour. "Cardiac lesions induced by 5-fluorouracil in the rabbit." Human & Experimental Toxicology 25, no. 6 (June 2006): 305–9. http://dx.doi.org/10.1191/0960327106ht628oa.

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Cardiotoxicity is a rare, but well-recognized complication of treatments with the anti-cancer drug 5-fluorouracil (5FU). The underlying mechanism, however, is not fully elucidated. A spasm of the coronary arteries is often considered to be the leading cause of myocardial ischemia and decreased contractility associated with 5FU. As spasm cannot account for all reported adverse cardiac effects, the present study was undertaken to search for alternative mechanisms. Groups of six rabbits were given either a single intravenous dose of 50 mg/kg 5FU or four intravenous doses of 15 mg/kg 5FU at 7-day intervals. A third group served as control. The heart was removed shortly after death or scheduled sacrifice of the animals, to perform macroscopic and microscopic examinations of the heart and to evidence apoptosis by the TUNEL method. Following a single dose of 50 mg/kg 5FU, all animals rapidly developed a massive hemorrhagic myocardial infarct with spasms of the proximal coronary arteries. Repeated infusions of 15 mg/kg 5FU induced left ventricular hypertrophy, foci of myocardial necrosis, thickening of intra-myocardial arterioles, and disseminated apoptosis in myocardial cells of the epicardium, as well as endothelial cells of the distal coronary arteries. These results indicate that a spasm of the coronary arteries is not the only mechanism of 5FU cardiotoxicity, and that apoptosis of myocardial and endothelial cells can result in inflammatory lesions mimicking toxic myocarditis.

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14

Zaccaro, L., A. M. Rossi, and R. Battolla. "Genotoxic action of 5-fluorouracil (5FU)." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 181, no. 2 (December 1987): 320. http://dx.doi.org/10.1016/0027-5107(87)90128-x.

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15

Lee, James J., Jan H. Beumer, and Edward Chu. "Therapeutic drug monitoring of 5-fluorouracil." Cancer Chemotherapy and Pharmacology 78, no. 3 (May 23, 2016): 447–64. http://dx.doi.org/10.1007/s00280-016-3054-2.

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16

Kopelman, Jerome N., and Kunio Miyazawa. "Inadvertent 5-fluorouracil treatment in early pregnancy: A report of three cases." Reproductive Toxicology 4, no. 3 (January 1990): 233–35. http://dx.doi.org/10.1016/0890-6238(90)90064-3.

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17

Stringer, Jessica M., Elyse O. K. Swindells, Nadeen Zerafa, Seng H. Liew, and Karla J. Hutt. "Multidose 5-Fluorouracil is Highly Toxic to Growing Ovarian Follicles in Mice." Toxicological Sciences 166, no. 1 (August 2, 2018): 97–107. http://dx.doi.org/10.1093/toxsci/kfy189.

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18

Oda, Y., K. Yamamoto, S. Nakamura, and I. Oki. "Induction of the SOS responses by 5-fluorouracil in Escherichia coli." Mutation Research/Environmental Mutagenesis and Related Subjects 147, no. 5 (October 1985): 270. http://dx.doi.org/10.1016/0165-1161(85)90106-2.

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19

Ohuchida, A., A. Furukawa, S. Umeno, H. Tamura, N. Horiya, T. Hara, M. Katoh, and T. Shibuya. "Effect of multiple treatments with 5-fluorouracil on the micronucleus test." Mutation Research/Environmental Mutagenesis and Related Subjects 252, no. 1 (February 1991): 100–101. http://dx.doi.org/10.1016/0165-1161(91)90296-k.

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20

Hong, C. Y., B. N. Chiang, J. Ku, and P. Wu. "Screening the in vitro Sperm-immobilizing Effect of some Anticancer Drugs." Human Toxicology 4, no. 4 (July 1985): 461–64. http://dx.doi.org/10.1177/096032718500400412.

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1 The in vitro sperm-immobilizing effect of seven anticancer agents, namely cyclophosphamide, 5-fluorouracil, cytarabine, mitomycin-C, 6-mercaptopurine, doxorubicin and vinblastine were screened with a transmembrane migration method. 2 Only doxorubicin and vinblastine inhibited human sperm motility. 3 Because colchicine, a microtubular inhibitor, had no sperm-immobilizing effect, we suggest that the sperm membrane is the site of action of these two anticancer drugs to inhibit human sperm motility.

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21

Berg, Stacey L., Frank M. Balis, Cynthia L. McCully, George A. Parker, Robert F. Murphy, and David G. Poplack. "Intrathecal 5-fluorouracil in the rhesus monkey." Cancer Chemotherapy and Pharmacology 31, no. 2 (1992): 127–30. http://dx.doi.org/10.1007/bf00685099.

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22

Lerner-Tung, Mary B., Alex Y. C. Chang, Ling S. Ong, and Deborah Kreiser. "Pharmacokinetics of intrapericardial administration of 5-fluorouracil." Cancer Chemotherapy and Pharmacology 40, no. 4 (June 17, 1997): 318–20. http://dx.doi.org/10.1007/s002800050663.

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23

Gaudreault, Jacques, Vanessa Shiu, Ann Bricarello, Brian J. Christian, Christina L. Zuch, and Barbara Mounho. "Concomitant Administration of Bevacizumab, Irinotecan, 5-Fluorouracil, and Leucovorin: Nonclinical Safety and Pharmacokinetics." International Journal of Toxicology 24, no. 5 (September 2005): 357–63. http://dx.doi.org/10.1080/10915810500209353.

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Bevacizumab (Avastin) is a humanized monoclonal antibody against vascular endothelial growth factor approved for use in combination with 5-fluorouracil (5-FU)-based chemotherapy for first-line treatment of metastatic colorectal cancer. The Saltz regimen (irinotecan/5-FU/leucovorin [LV]) is a first-line treatment for this indication. The objective of this study was to evaluate the safety of bevacizumab when administered concomitantly with the Saltz regimen to cynomolgus monkeys, and to determine if the pharmacokinetics of bevacizumab, irinotecan, SN38 (the active metabolite of irinotecan), or 5-FU were affected by combined administration. Male cynomolgus monkeys were intravenously administered the Saltz regimen (125 mg/m2 irinotecan, 500 mg/m2 5-FU, 20 mg/m2 LV) alone ( n = 4) or concomitantly with 10 mg/kg bevacizumab ( n = 5) on days 1 and 8. All animals survived to euthanasia on day 15. Adverse effects associated with the Saltz regimen included diarrhea and neutropenia. Macroscopically, two animals from each group had small thymus glands that correlated microscopically with lymphoid depletion. Myeloid hypoplasia and/or erythroid hyperplasia was observed in the sternal bone marrow of most animals. These effects were considered to be associated with the Saltz regimen; concomitant bevacizumab administration did not alter the severity of these findings. Irinotecan and 5-FU were observed to be rapidly eliminated ( t1/2 = 1 h and 0.5 h, respectively). Although the number of animals in each group was small and no statistical comparison between groups was performed, bevacizumab did not affect the disposition of either agent. These results indicate that bevacizumab can be safely administered in combination with the Saltz regimen without pharmacokinetic interaction.

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24

Grafton, Thomas F., Johnny J. Bazare, Deborah K. Hansen, and Daniel M. Sheehan. "The in vitro embryotoxicity of 5-fluorouracil in rat embryos." Teratology 36, no. 3 (December 1987): 371–77. http://dx.doi.org/10.1002/tera.1420360314.

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25

Stupans, I., D. A. Richards, and M. T. McClure. "Effects of 5-fluorouracil treatment on rat liver microsomal enzymes." Xenobiotica 25, no. 1 (January 1995): 1–8. http://dx.doi.org/10.3109/00498259509061827.

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26

Nakamura, Minoru, Farrel L. Fort, and Yasumoto Kikuchi. "Fetal liver micronucleus assay in mice of 5-fluorouracil and related compounds." Mutation Research/Environmental Mutagenesis and Related Subjects 291, no. 1 (February 1993): 29–34. http://dx.doi.org/10.1016/0165-1161(93)90014-q.

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27

Wang, Jun, Wei Liu, Qing Zhao, Qi Qi, Na Lu, Yong Yang, Fei-Fei Nei, Jing-Jing Rong, Qi-Dong You, and Qing-Long Guo. "Synergistic effect of 5-fluorouracil with gambogic acid on BGC-823 human gastric carcinoma." Toxicology 256, no. 1-2 (February 2009): 135–40. http://dx.doi.org/10.1016/j.tox.2008.11.014.

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28

Robbins, Terry J., Donnell Bowen, Quang Q. Bui, and Minh-Tam Tran. "Modulation of high-dose methotrexate toxicity by a non-toxic level of 5-fluorouracil." Toxicology 41, no. 1 (October 1986): 61–73. http://dx.doi.org/10.1016/0300-483x(86)90104-6.

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29

Gao, Liping, Runyu Ma, Junbo Zhou, and Shuzhen Cheng. "Changes of Serum Erythropoietin During Cisplatin- or 5-Fluorouracil-Induced Anemia in Rats." Toxicology Mechanisms and Methods 16, no. 9 (January 2006): 501–6. http://dx.doi.org/10.1080/15376510600751962.

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30

Shuey, Dana L., Robert M. Zucker, Kenneth H. Elstein, and John M. Rogers. "Fetal anemia following maternal exposure to 5-fluorouracil in the rat." Teratology 49, no. 4 (April 1994): 311–19. http://dx.doi.org/10.1002/tera.1420490411.

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31

Oda, Yoshimitsu. "Induction of SOS responses in Escherichia coli by 5-fluorouracil." Mutation Research/DNA Repair Reports 183, no. 2 (March 1987): 103–8. http://dx.doi.org/10.1016/0167-8817(87)90051-4.

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32

Milano, G., A. Thyss, J. Santini, M. Frenay, E. Francois, M. Schneider, and F. Demard. "Salivary passage of 5-fluorouracil during continuous infusion." Cancer Chemotherapy and Pharmacology 24, no. 3 (September 1989): 197–99. http://dx.doi.org/10.1007/bf00300243.

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33

Eatock, M. M., W. Carlin, D. J. Dunlop, M. Soukop, and D. G. Watson. "Bioavailability of subcutaneous 5-fluorouracil: a case report." Cancer Chemotherapy and Pharmacology 38, no. 1 (March 28, 1996): 110–12. http://dx.doi.org/10.1007/s002800050456.

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34

Li, Yuai, Greg A. Looney, Bruce F. Kimler, and A. Hurwitz. "Opiate effects on 5-fluorouracil disposition in mice." Cancer Chemotherapy and Pharmacology 39, no. 3 (December 2, 1996): 273–77. http://dx.doi.org/10.1007/s002800050572.

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35

Helsby, N. A., W. Y. Lo, P. Thompson, and G. R. Laking. "Do 5-fluorouracil therapies alter CYP2C19 metaboliser status?" Cancer Chemotherapy and Pharmacology 66, no. 2 (February 17, 2010): 405–7. http://dx.doi.org/10.1007/s00280-010-1277-1.

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36

Thiberville, Luc, Patricia Compagnon, Nicholas Moore, Gerard Bastian, Marie-Odile Richard, Marie-France Hellot, Colette Vincent, et al. "Plasma 5-fluorouracil and ?-fluoro-?-alanin accumulation in lung cancer patients treated with continuous infusion of cisplatin and 5-fluorouracil." Cancer Chemotherapy and Pharmacology 35, no. 1 (1994): 64–70. http://dx.doi.org/10.1007/bf00686286.

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37

Thiberville, L., Patricia Compagnon, Nicholas Moore, Gerard Bastian, Marie-Odile Richard, Marie-France Hellot, Colette Vincent, et al. "Plasma 5-fluorouracil and ?-fluoro-?-alanin accumulation in lung cancer patients treated with continuous infusion of cisplatin and 5-fluorouracil." Cancer Chemotherapy and Pharmacology 35, no. 1 (November 1, 1994): 64–70. http://dx.doi.org/10.1007/s002800050194.

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38

Khor, S. P., H. Amyx, Stephen T. Davis, Donald Nelson, David P. Baccanari, and Thomas Spector. "Dihydropyrimidine dehydrogenase inactivation and 5-fluorouracil pharmacokinetics: allometric scaling of animal data, pharmacokinetics and toxicodynamics of 5-fluorouracil in humans." Cancer Chemotherapy and Pharmacology 39, no. 3 (December 2, 1996): 233–38. http://dx.doi.org/10.1007/s002800050566.

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39

Elstein, Kenneth H., M. Leonard Mole, R. Woodrow Setzer, Robert M. Zucker, Robert J. Kavlock, John M. Rogers, and Christopher Lau. "Nucleoside-Mediated Mitigation of 5-Fluorouracil-Induced Toxicity in Synchronized Murine Erythroleukemic Cells." Toxicology and Applied Pharmacology 146, no. 1 (September 1997): 29–39. http://dx.doi.org/10.1006/taap.1997.8208.

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40

Erdem, Burak, Serhat Imamoglu, and Nimet Yesim Ercalik. "Needling with 5-fluorouracil for encapsulated blebs after Ahmed glaucoma valve implantation." Cutaneous and Ocular Toxicology 38, no. 4 (August 12, 2019): 395–400. http://dx.doi.org/10.1080/15569527.2019.1650060.

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41

Gielen, Marcel, Huairang Ma, Abdeslam Bouhdid, Hassan Dalil, Monique Biesemans, and Rudolph Willem. "Di-n-Butyl-, Tri-n-Butyl- and Triphenyltin dl-Terebates: Synthesis, Characterization and In Vitro Antitumour Activity." Metal-Based Drugs 4, no. 4 (January 1, 1997): 193–97. http://dx.doi.org/10.1155/mbd.1997.193.

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Di-n-butyltin, tri-n-butyltin and triphenyltin terebates were screened against several human tumour cell lines and found comparably or more active than carboplatin, cis-platin, 5-fluorouracil, methotrexate and doxorubicin, some reference compounds used clinically.

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42

Kim, Joon Ki, Kyoung Ah Kang, Mei Jing Piao, Yea Seong Ryu, Xia Han, Pattage Madushan Dilhara Jayatissa Fernando, Min Chang Oh, et al. "Endoplasmic reticulum stress induces 5-fluorouracil resistance in human colon cancer cells." Environmental Toxicology and Pharmacology 44 (June 2016): 128–33. http://dx.doi.org/10.1016/j.etap.2016.05.005.

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43

Hassan, Abdulhameed Abdulmajeed, Marwan Salah Salman, and Mazin GH H. AL-Badri. "Pterygium Excision Using Bare Sclera Technique and Adjunctive 5-Fluorouracil Application." Indian Journal of Forensic Medicine & Toxicology 13, no. 4 (2019): 480. http://dx.doi.org/10.5958/0973-9130.2019.00336.0.

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44

Weng, Qinjie, Biqin Tan, Jiajia Wang, Jing Wang, Hui Zhou, Jing Shi, QiaoJun He, and Bo Yang. "5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice." Toxicology 325 (November 2014): 144–50. http://dx.doi.org/10.1016/j.tox.2014.08.011.

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45

Cohen, Philip R. "Chronic cutaneous lupus erythematosus induced by 5-fluorouracil." Expert Review of Clinical Pharmacology 13, no. 8 (July 17, 2020): 917–18. http://dx.doi.org/10.1080/17512433.2020.1793669.

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46

Strike, David G., William Bonnez, and Richard C. Reichman. "Comment: papillomaviruses not in herpes group; fluorouracil in condyloma." Drug Intelligence & Clinical Pharmacy 21, no. 6 (June 1987): 549. http://dx.doi.org/10.1177/106002808702100622.

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47

Bolli, E., S. Saccomanno, G. Mondini, C. Aschele, A. Guglielmi, B. Ligas, M. Connio, et al. "5-Fluorouracil plus 5-methyltetrahydrofolate in advanced pancreatic cancer." Cancer Chemotherapy and Pharmacology 35, no. 4 (January 1, 1995): 339–42. http://dx.doi.org/10.1007/s002800050243.

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48

Isard, P. F., and S. G. Rosolen. "5 Fluorouracil Insert Associated with Gonioconjunctival Shunt in Glaucoma Surgery on Cat: Preliminary Results." Journal of Toxicology: Cutaneous and Ocular Toxicology 18, no. 3 (January 1999): 268–69. http://dx.doi.org/10.3109/15569529909044249.

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49

Al-Asmari, AK, AM Al-Zahrani, AQ Khan, HM Al-Shahrani, and M. Ali Al Amri. "Taurine ameliorates 5-flourouracil-induced intestinal mucositis, hepatorenal and reproductive organ damage in Wistar rats." Human & Experimental Toxicology 35, no. 1 (February 27, 2015): 10–20. http://dx.doi.org/10.1177/0960327115573597.

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5-Fluorouracil is one of the most commonly used anticancer drugs for the treatment of various types of cancer but has potential adverse effects such as intestinal mucositis, renal, hepatic, and reproductive organ toxicity. Attention has been given to approaches to reduce the side effects and improve the therapeutic effectiveness of chemotherapeutic drugs. In this study, we have investigated the protective effect of taurine (Tau) on 5-fluorouracil (5-FU) induced adverse effects in Wistar rats. Animals were divided into four groups with six animals ( n = 6) in each group. Group I received vehicle only and served as control group. Groups II, III, and IV animals were given oral gavage of 5-FU at 50 mg/kg body weight for 4 days. Tau was given to the animals of groups III and IV 30 min prior to 5-FU administration. We observed marked elevation in the myeloperoxidase (MPO) activity after 5-FU administration, which was reversed by Tau pretreatment. Histological observation of liver, kidney, intestine, testis, and prostate revealed that 5-FU administration resulted in anomalies like distortion of normal cellular architecture, infiltration of inflammatory cells, and loss of cellular integrity. These histopathological changes were markedly suppressed by Tau treatment. In conclusion, biochemical and histological findings of this study suggest that Tau has strong preventive potential against complications of anticancer drug 5-FU and hence Tau may play an important role in combinational chemotherapy to enhance the therapeutic efficacy of anticancer drugs.

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Tyagi, Sadhna, Sukh Mahendra Singh, Sujan Gencaslan, W. S. Sheldrick, and Udai P. Singh. "Metal–5-Fluorouracil–Histamine Complexes: Solution, Structural, and Antitumour Studies." Metal-Based Drugs 8, no. 6 (January 1, 2002): 337–45. http://dx.doi.org/10.1155/mbd.2002.337.

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Abstract:

Solution studies were performed pH-metrically to study the interaction of Co(II), Ni(II), Cu(II), Zn(II) and Cd(II) metal ions with 5-fluorouracil (5FU) and histamine (Hm) separately (binary) and in the presence of each other (ternary) at 25±0.1 C° temperature and a constant ionic strength of 0.1 M NaNO3 in aqueous solution. The ternary complexes have been found to be more stable than the corresponding binary complexes as shown by the positive value of Δlog⁡K. The species distribution curves have been obtained using the computer programme BEST. On the basis of species distribution results, efforts were also made to prepare some mixed complexes of Co(II), Ni(II), Cu(II), Zn(II) and Cd(II) ions by performing the reaction of their metal nitrates, 5FU and Hm in aqueous ethanol medium at suitable pH. The isolated solid complexes were characterized by different physico-chemical method in order to suggest the possible binding site of the ligands and the structure of the resultant complexes. All these complexes were checked for their antitumour activity by injecting in Dalton's lymphoma (DL) and Sarcoma-180 (S-180) bearing C3H/He mice. The results indicate that some complexes have good antitumour activity both in vivo and in vitro.

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