Renal carcinogen

Goldsworthy TL, Lyght O, Burnett VL, et al. 1988. Potential role of alpha-2y-globulin, protein droplet accumulation, and cell replication in the renal carcinogenicity of rats exposed to trichloroethylene, perchloroethylene, and pentachloroethane. Toxicol Appl Pharmacol 96 367-379. 

McLaren J, Boulikas T, Vamvakas S. 1994. Induction of poly(ADP-ribosyl)ation in the kidney after in vivo application of renal carcinogens. T oxicology 88 101-112. 

Target Organ Toxicity. This section focuses on mechanisms for sensitive health effects of major concern for lead—cardiovascular effects, hematological effects, and neurological effects, particularly in children. Bone is a major sink for lead, and there is some limited information regarding the effects of lead on bone and potential mechanisms of action. Renal effects occur at relatively high blood lead levels and evidence of renal carcinogenicity has been demonstrated only in animals mechanisms for these effects will be discussed briefly. 

Dekant, W., 1993, Bioactivation of nephrotoxins and renal carcinogens by glutathione S-conjugate formation. Toxicol. Lett. 67 151-160 Dooley, D.M., 1999, Stmcture and biogenesis oftopaquiones and related cofactors. J. Biol. Inorg. Chem. 4 1-11... 

Klos C, Dekant W. 1994. Comparative metabolism of the renal carcinogen 1,4,-dichlorobenzene in rat Identificaiton and quantitation of metabolites. Xenobiotica 24(10) 965-976. 

The selective renal carcinogenicity of dichloroacetylene may be due to a bioactivation mechanism that involves glutathione S-conju-gate formation, translocation to the kidneys, and subsequent renal metabolism to yield reactive electrophiles presumably responsible for carcinogenicity. ... 

Noguchi M, Nomata K, Watanabe J, Kanetake H, Saito Y. Changes in gap junction intercellular communication in renal tubular epithelial cell in vitro treated with renal carcinogens. Cancer Letts 1998 122 77-84. 

K6. Kasai, H., Nishimura, S., Kurokawa, Y., and Hayashi, Y., Oral administration of the renal carcinogen, potassium bromate, specifically promotes 8-hydroxydeoxy-guanosine in rat target DNA. Carcinogenesis 8, 1959-1961 (1987). 

Toyokuni S, Uchida K, Okamoto K, Hattori-Nakakuki Y, Hiai H, Stadt-man ER (1994) Fonnation of 4-hydi oxy-2-nonenal-modified proteins in tire renal proximal tubules of icits treated with a renal carcinogen, feiiic nitiilotiiacetate. Proc Natl Acad Sci USA 91 2616-2620. 

Calomel can generate reactive oxygen species and deplete glutathione levels. Both genotoxic and nongenotoxic mechanisms may contribute to renal carcinogenic effect of mercury. 

Einally, the renal carcinogenicity of potassium bromate was examined using a two-stage carcinogenesis model. A total of 240 male Wistar rats were treated with iV-ethyl-A-hydroxyethylnitrosamine for the initiahon of kidney carcinogenesis and were thereafter administered potassium bromate at doses of 0, 0.02, 0.2, 2, 8, 30, 125, and 500ppm in their drinking water for 16 weeks (Wei et al. 2009) Due to... 

The results of these two sets of experiments support the conclusion that there is a no-effect level and threshold dose for potassium bromate renal carcinogenicity in the rat. 

Lock, E. A., and Hard, G. C. (2004). Chemically induced renal tubule tumors in the laboratory rat and mouse Review of the NCI/NTP database and categorization of renal carcinogens based on mechanistic information. CritRev Toxicol 34, 211-299. 

Toyokuni, S. et al.. Treatment of Wistar rats with a renal carcinogen, ferric nitrilotriacetate, causes DNA-protein cross-linking between thymine and tyrosine in their renal chromatin, Int J. Cancer, 62 (3), 309, 1995. 

Kurokawa, Y., Maekawa, A., Takahashi, M., and Hayashi, Y, Toxicity and carcinogenicity of potassium bromate-a new renal carcinogen. Environ. Health Perspect., 87, 309, 1990. 

Induction of poly(ADP-ribosyl)ation was reported in the kidney after in vivo application of renal carcinogens such as trichloroethene and dichloroacetylene subsequent to DNA double-strand breaks. Potassium bromate and ferric nitrilotriacetate, whose nephrotoxicity is thought to result from ROS formation, both induced poly(ADP-ribosyl)ation with the concomitant formation of DNA double-strand breaks. Recendy, PARP activation has been associated with both gentamicin and cisplatin-induced nephrotoxicity.Both types of nephrotoxicity involve the generation of ROS and the beneficial effects of different therapeutic approaches aimed at reducing ROS formation have been evaluated. 

Limonciel, A. and Jennings, P. (2014) A review of the evidence that ochratoxin A is an Nrf2 inhibitor implications for nephrotoxicity and renal carcinogenicity. Toxins 6, 371-379. 

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