Kidneys damage in rats

Derived from lowest observable adverse effect level (LOAEL) of 42 pg Hg/kg BW daily of phenylmercuric acetate tor detectable kidney damage in rats after 2 years and an uncertainty factor of 5 (USPHS 1994). 

As mentioned earlier, deamidation by excessive protein hydrolysis is undesirable for food use because it could result in reduced protein functionality and the release of bitter-tasting peptides [19]. Alkali-catalyzed deamidation is also undesirable because, in addition to indiscriminate hydrolysis, alkali treatment results in products such as lysinoalanine that have been implicated in kidney damage in rats [20,21],... 

Chronic-Duration Exposure and Cancer. No studies were located in humans following chrome-duration exposure to hexachloroethane for any exposure route. No chronic animal studies were conducted using the inhalation route of exposure. In oral studies with rats, the kidney was identified as a primary target organ in males and females (NTP 1989). The kidney damage in male rats was the result of hyaline droplet nephropathy and, accordingly, was not suitable as the basis for an oral MRL. In contrast to acute- and intermediate-duration oral exposure, liver toxicity was not evident in rats following chronic oral exposure. There were no studies of chronic dermal exposure to hexachloroethane. 

Toxicology. p-Chloro-m-cresol (PCMC) causes kidney damage in male rats after chronic exposure. 

Intermediate-Duration Exposure. No data are available on the effects of hexachlorobutadiene in humans after intermediate-duration inhalation, oral, or dermal exposures. In animals, data on inhalation exposure are limited to one developmental toxicity study in rats in which maternal body weights were reduced at a concentration (15 ppm) that was also fetotoxic (Saillenfait et al. 1989). Oral studies revealed kidney damage in female mice at dose levels of 0.2 mg/kg/day (NTP 1991 Yang et al. 1989). This LOAEL was used to derive an intermediate-duration oral MRL of 0.0002 mg/kg/day. 

Di(2-ethylhexyl) adipate did not bind covalently to mouse liver DNA in vivo. One report showed evidence of oxidative damage in rat liver DNA in vivo but not in rat kidney DNA. A weak dominant lethal effect has been reported in male mice. Analyses of mouse bone marrow after treatment with di(2-ethylhexyl) adipate in vivo found no induction of micronuclei in one study and no induction of chromosomal aberrations in one study. Urine from rats treated with di(2-ethylhexyl) adipate by gavage was not mutagenic to Salmonella typhimurium. 

Yamada K, SugIsakI Y, Akimoto M, Yamanaka N. FK506-induced juxtaglomerular apparatus hyperplasia and tubular damage In rat kidney-morphologic and biologic analysis. Transplant Proc 1992 24 1396-1398. 

Toxicity. The renal toxicity of (14), (18) and (19) has been studied in mice and all were found less toxic than cisplatin [48, 74]. Spiroplatin (14) was also shown to be without renal toxicity in rats, but the compound caused severe kidney damage in dogs [112, 114]. 

Cottrell, R. C., C. E. Agrelo, S. D. GangoUi, and P. Grasso. 1976. Histochemical and biochemical studies of chemically induced acute kidney damage in the rat. Food Cosmetics Toxicology 14 593-598. 

Saravanan, N., and N. Nalini. 2007b. Impact of Hemidesmus indicus R.Br. extract on ethanol-mediated oxidative damage in rat kidney. Redox Rep. 12(5) 229-235. 

The occurrence of oxidative DNA damage was investigated in vivo in male Fischer 344 rats dosed orally with ochratoxin A at 0, 0.03, 0.1 or 0.3 mg/kg bw per day for 4 weeks. The doses used were within the range known to have caused kidney tumours in rats in a 2-year study. Oxidative DNA damage was assessed by the comet assay, with and without use of the repair enzyme Fpg. There was no effect on basic DNA damage, but oxidative DNA damage was detected with Fpg treatment in kidney and liver at all doses tested (Kamp et al., 2005b). 

Ozcelik, N., Soyoz, M. Kilinc, I. (2004) Effects of ochratoxin A on oxidative damage in rat kidney protective role of melatonin. J. Appl. Toxicol. 24, 211-215. 

The properties of cyanuric acid are similar to melamine, with its LDj, for ingestion in rats being 7700 mg/kg of body weight. From the human body, 98% of cyanuric acid is excreted within 24 h. Cyanuric acid causes kidney damage in animals, and the NOAEL value was found to be 150 mg/kg of body weight per day. 

Fugmann, T., Borgia, B., Revesz, C., Godo, M., Forsblom, C., Hamar, P., Holthofer, H., Neri, D., and Roesli, C., 2011. Proteomic identification of vanin-1 as a marker of kidney damage in a rat model of type 1 diabetic nephropathy. Kidney International. 80 272-281. 

In low-level chronic exposure, MX sequesters cadmium intracellularly as the cadmium-MT complex and thereby decreases the toxic effects of the metal. By contrast, extracellular cadmium-MX has been shown to be nephrotoxic to experimental animals. Parenteral injection of cadmium in the form of cadmium-MT can cause acute renal damage in rats and mice (Nordberg et al. 1975 Cherian et al. 1976 Squibb et al. 1984 Maitani et al. 1988). These toxic effects were similar to those observed after repeated exposure to cadmium salts but the critical renal concentration of cadmium is much lower after injection of cadmium-MX (10//g/g) than after repeated injections of cadmium salts (200//g/g). The low molecular weight cadmium-MX is freely filtered by the glomerulus and reabsorbed by the proximal convoluted tubules and can cause acute damage to the renal tubular epithelial cells (Cherian et al. 1976 Goyer et al. 1984 Dorian et al. 1992). It has been proposed that the hepatic cadmium-Mt is released and transported to kidney in blood plasma and that the nephrotoxicity occurs at a certain renal concentration of cadmium with chronic exposure (Goyer et al. 1978, 1984 Dudley et al. 1985). In a recent liver transplant experiment, the movement of cadmium-MX form liver to kidney was demonstrated in rats where the liver with cadmium-MX was transplanted to a control rat (Chan et al. 1993). 

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