| Wechselwirkungen | The injection to rats of glycerol, cisplatin, uranyl acetate, sodium dichromate, and mercuric chloride is followed on the third day by acute renal failure. A new approach for quantitative estimation of disturbance of excretory renal function is presented. The decrease in renal function due to uranyl acetate was 77%sodium dichromate, 71%mercuric chloride, 52%cisplatin, 25%and glycerol, 10%. The kidneys still maintained serum ion concentration close to normal values. Injection of nephrotoxic drugs increased kidney wet weight by 24-57%. This was caused by swelling of renal tissue and increases in dry weight of the kidneys. The sodium content increased in the renal cortex and decreased in the papilla. The potassium content of the renal cortex is increased. The effect of some nephrotoxic drugs is suggested to depend on an increased number of cells in the renal cortex (probably due to hemostasis and inflammation) and a decrease of renal medulla function. The above drugs induce disturbance of kidney tissue but have no effect on the ion and water content in liver and m. gastrocnemius.Cactus (Opuntia ficus-indica) is a xerophyte plant that belongs to the Cactaceae family. The present study was designed to investigate the possible protective effects of cactus cladodes extract (CCE) on sodium dichromate-induced testis damage in adult male Wistar rats. For this purpose, CCE at a dose of 100 mg/kg was orally administrated, followed by 10 mg/kg sodium dichromate (intraperitoneal injection). After 40 days of treatment, the rats were sacrificed, and the testes were excised for histological, lipid peroxidation (LPO), and antioxidant enzyme analyses. Sodium dichromate treatment significantly (P<0.01) decreased the body, testis, and accessory sex organ weights, sperm count and motility, and serum testosterone level. In addition, histological analysis revealed pronounced morphological alterations with tubular necrosis and reduction in the number of gametes in the lumen of the seminiferous tubules of sodium dichromate-intoxicated rats. Furthermore, exposure to sodium dichromate significantly (P<0.01) increased LPO level and decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in testis. Interestingly, pretreatment with CCE significantly (P<0.01) restored the serum testosterone level, sperm count, and motility to the levels of the control group. Moreover, CCE administration was capable of reducing the elevated level of LPO and significantly (P<0.01) increased SOD, CAT, and GPx activities in testis. Cactus cladodes supplementation minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by sodium dichromate in the rat testis.Antioxidants of the vitamin E family have protective effects against metal toxicity. We examined the protective effect of racemic LLU-alpha [2,7,8-trimethyl-2-(carboxyethyl)-6-hydroxychroman] a metabolite of gamma-tocopherol, in comparison to the effect of alpha- and gamma-tocopherol in rats treated with sodium dichromate (Cr) or thallium sulfate (Tl). We measured metal nephrotoxicity based on urinary protein excretion and discussed it with respect to the metal concentration in renal tissue. The ranking of antioxidant activity (iron stimulated lipid peroxidation, luminol and lucigenin amplified chemiluminescence) was determined in the following order: alpha-tocopherol<gamma-tocopherol<LLU-alpha. Pretreatment with LLU-alpha produced lower chromate nephrotoxicity than alpha- or gamma-tocopherol, but did not influence Cr concentration in renal tissue. The protective effect of LLU-alpha against Cr toxicity seemed to be caused by its stronger antioxidant activity in comparison to alpha- and gamma-tocopherol. Pretreatment with LLU-alpha resulted in lower thallium-induced proteinuria, a lower concentration of Tl in the renal medulla, and higher urinary Tl excretion. Unlike LLU-alpha, which has been shown to inhibit K(+) channels in the apical membrane of the thick ascending limb of Henle's loop, we found that gamma-tocopherol did not. This finding reaffirmed the similarity between K(+) and Tl(+) and also explained the significantly decreased Tl concentration in the renal medulla in rats treated with LLU-alpha. We speculate that the protective effect of LLU-alpha against Tl nephrotoxicity is caused both by its antioxidant effect and, at least in part, by its ability to decrease Tl concentration as a consequence of inhibited Tl(+) uptake through K(+) channels. This finding confirmed the similarity between K(+) and Tl(+) and also explained the significantly decreased Tl concentration in the renal medulla in rats treated with LLU-alpha.Genotoxic effects of xenobiotics are a possible step in tumor initiation in the mucosa of the upper aerodigestive tract. Using the comet assay, detecting genotoxicity in human tissue has been restricted to single incubations in vitro, but in vivo most xenobiotics harm their target in a repetitive or chronic manner. Therefore, we propose a model, which provides repetitive incubations in human upper aerodigestive tract mucosa cultures. Samples of human inferior nasal turbinate mucosa (n = 25) were cultured according to a modified version of a technique originally described by Steinsvag. On day 1 fresh samples and on days 7, 9 and 11 organ cultures were incubated with N-nitrosodiethylamine (NDEA), sodium dichromate (Na2Cr2O7) and N'-methyl-N-nitro-N-nitrosoguanidine (MNNG). Mucosa samples and organ cultures, respectively, underwent a modified comet assay on days 1, 7 and 11. Genotoxicity could be shown for NDEA, Na2Cr2O7 and MNNG on days 1, 7 and 11. Duration of tissue culture and repetitive incubations did not significantly influence the results for NDEA. Nevertheless, Na2Cr2O7 and MNNG caused higher genotoxic effects on cultures subjected to the comet assay on day 11. This model may help to assess genotoxic hazards posed by environmental pollutants that have a cumulative character in repetitive or chronic exposure in vivo.For more Interactions (Complete) data for SODIUM DICHROMATE (14 total), please visit the HSDB record page. |
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