Effect of zinc pretreatment on mercuric chloride-induced lipid peroxidation in the rat kidney

Fukino, Hideki; Hirai, Masami Yokota; Hsueh, Yu Mei; Yamane, Yasuhiro

doi:10.1016/0041-008x(84)90091-7

Cited by 80 publications

(23 citation statements)

References 17 publications

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“…Our results thus indicate that there is a prooxidant activity observed on the part of selenium in mercury treated animals. We have selected the dose of mercuric chloride on the basis of study by Fukino who used 15 µmoles mercury in rats 44) , which was slightly lower than our dose and the dose of selenium was taken in a way to provide 1:1 molar ratio with the dose of mercury. This may have provided higher selenium dose to produce selenium toxicity in combination with mercury due to the action on thiols to generate superoxides and reactive oxygen species, similar results were reported by Spallholz 45) .…”

Section: Discussionmentioning

confidence: 99%

Role of Selenium in Mercury Intoxication in Mice

Agarwal

Behari

2007

Ind Health

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Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 µ µ µ µ µmole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.

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Section: Discussionmentioning

confidence: 99%

Role of Selenium in Mercury Intoxication in Mice

Agarwal

Behari

2007

Ind Health

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“…Alteration in levels of malondialdehyde (MDA, nmole/g wet tissue) was used as an index of LPO according to the procedure using thiobarbituric acid (TBA) (76). The TBA method has been used extensively to measure LPO levels in the liver, and its recent application to the kidney allowed dose-dependent and time-dependent changes to be shown in response to exogenous chemicals (77)(78)(79).…”

Section: Gsh ( MM )mentioning

confidence: 99%

Toxicity and Carcinogenicity of Potassium Bromate: A New Renal Carcinogen

Kurokawa¹,

Maekawa²,

Takahashi³

et al. 1990

Environmental Health Perspectives

150

130

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Potassium bromate (KBrO3) is an oxidizing agent that has been used as a food additive, mainly in the bread-making process. Although adverse effects are not evident in animals fed bread-based diets made from flour treated with KBrO3, the agent is carcinogenic in rats and nephrotoxic in both man and experimental animals when given orally. It has been demonstrated that KBrO3 induces renal cell tumors, mesotheliomas of the peritoneum, and follicular cell tumors of the thyroid. In addition, experiments aimed at elucidating the mode of carcinogenic action have revealed that KBrO3 is a complete carcinogen, possessing both initiating and promoting activities for rat renal tumorigenesis. However, the potential seems to be weak in mice and hamsters. In contrast to its weak mutagenic activity in microbial assays, KBrO3 showed relatively strong potential inducing chromosome aberrations both in vitro and in vivo. Glutathione and cysteine degrade KBrO3 in vitro; in turn, the KBrO3 has inhibitory effects on inducing lipid peroxidation in the rat kidney. Active oxygen radicals generated from KBrO3 were implicated in its toxic and carcinogenic effects, especially because KBrO3 produced 8-hydroxydeoxyguanosine in the rat kidney. A wide range of data from applications of various analytical methods are now available for risk assessment purposes.

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“…Hg 2+ reacts with thiol groups (-SH), thus depleting intracellular thiols, especially glutathione, and causing cellular oxidative stress or predisposing cells to it (3). Other antioxidants, including ascorbic acid and vitamin E, have been reported to be depleted in HgCl 2 -treated rats (4). If animals are pretreated with superoxide dismutase (Cu,Zn-SOD) before acute intoxication is induced, histological changes are prevented (5).…”

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confidence: 99%

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

Gutiérrez-Carrasquilla

Mazzotti

Araújo

et al. 2006

Braz J Med Biol Res

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The present study was designed to evaluate the time course changes in peripheral markers of oxidative stress in a chronic HgCl 2 intoxication model. Twenty male adult Wistar rats were treated subcutaneously daily for 30 days and divided into two groups of 10 animals each: Hg, which received HgCl 2 (0.16 mg kg -1 day -1 ), and control, receiving the same volume of saline solution. Blood was collected at the first, second and fourth weeks of Hg administration to evaluate lipid peroxidation (LPO), total radical trapping antioxidant potential (TRAP), and superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase (CAT). HgCl 2 administration induced a rise (by 26%) in LPO compared to control (143 ± 10 cps/mg hemoglobin) in the second week and no difference was found at the end of the treatment. At that time, GST and GPx were higher (14 and 24%, respectively) in the Hg group, and Cu,Zn-SOD was lower (54%) compared to control. At the end of the treatment, Cu,Zn-SOD and CAT were higher (43 and 10%, respectively) in the Hg group compared to control (4.6 ± 0.3 U/mg protein; 37 ± 0.9 pmol/mg protein, respectively). TRAP was lower (69%) in the first week compared to control (43.8 ± 1.9 mM Trolox). These data provide evidence that HgCl 2 administration is accompanied by systemic oxidative damage in the initial phase of the process, which leads to adaptive changes in the antioxidant reserve, thus decreasing the oxidative injury at the end of 30 days of HgCl 2 administration. These results suggest that a preventive treatment with antioxidants would help to avoid oxidative damage in subjects with chronic intoxication.

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Effect of zinc pretreatment on mercuric chloride-induced lipid peroxidation in the rat kidney

Cited by 80 publications

References 17 publications

Role of Selenium in Mercury Intoxication in Mice

Role of Selenium in Mercury Intoxication in Mice

Toxicity and Carcinogenicity of Potassium Bromate: A New Renal Carcinogen

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

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