[Experimental study on the effects of BSO, GSH, vitamin C and DMPS on the nephrotoxicity induced by mercury].
OBJECTIVE
To study the renal toxicity caused by mercury administrated once and to observe the effects of buthionine sulfoximine (BSO), gluthionein (GSH), vitamin C (VC), and sodium 2,3-dimercato-1-propanesulfonate (DMPS) pretreatment on the nephrotoxicity of mercury.


METHODS
Sixty-four Wistar rats were divided randomly into eight groups, i. e., control group, low, middle and high dose mercury groups and BSO, GSH, VC, DMPS pretreatment groups. The low, middle, and high dose mercury group rats were subcutaneously (sc) injected with 0.75, 1.5, and 2.5 mg/kg HgCl2, respectively. The BSO pretreatment group rats were intraperitoneally (ip) injected with 0.5 mmol/kg BSO and four hours later sc administrated with 0.75mg/kg HgCl2. The GSH, VC and DMPS pretreatment group rats were ip injected with 3 mmol/kg GSH, 4mmol/kg VC, 200 micromol/kg DMPS, respectively, and two hours later sc administrated with 2.5 mg/kg HgCl2. The control group rats were sc injected with saline at corresponding time. The volume of injection was 5 ml/kg body weight. The 12 h urine samples were collected after 12 hours. After 48 hours, the blood samples were collected and then centrifuged to get the serum. The liver and renal cortex were also removed. Mercury contents in the liver, renal cortex, and urine samples were measured. Urinary NAG, ALP, LDH activities, urinary protein and BUN contents were also determined.


RESULTS
Mercury concentrations in the liver, renal cortex, and urine samples increased with mercury dose increasing. Mercury contents in the renal cortex presented evident dose-effect relationship. Mercury concentrations in the liver of high-dose mercury group were higher significantly than that of low, middle-dose mercury group, and control group. The concentrations of urinary mercury in the middle and high dose mercury groups were higher significantly than that of control group. Compared with 0.75mg/kg HgCl2 alone group, BSO pretreatment increased mercury concentrations in the liver, but decreased the concentrations in the renal cortex and urine. Mercury concentrations in the liver of GSH, VC and DMPS pretreatment groups were lower than that of 2.5 mg/kg HgCl2 alone group. Urinary NAG, ALP, LDH activities, urinary protein and BUN contents increased with mercury dose increasing, and the values in the animals of 2.5 mg/kg HgCl2 mercury group were higher significantly than that of control, 0.75 and 1.5 mg/kg HgCl2 groups. Urinary NAG, ALP activities, urinary protein and BUN contents in the rats of BSO pretreatment were higher than that of 0.75 mg/kg HgCl2 alone group and control group. Compared with 2.5 mg/kg HgCl2 alone group, urinary NAG, ALP, LDH activities, urinary protein and BUN contents decreased significantly.


CONCLUSIONS
Mercury concentrations in the liver, renal cortex, and urine of the rats increased with mercury dose increasing. BSO pretreatment could enhance the renal toxicity induced by mercury, however, GSH, VC, and DMPS pretreatment had antagonistic effects on nephrotoxicity of the mercury.
Zhao-Fa
Xu
X
School of Public Health, China Medical University, Shenyang 110001, China.
Jing-Hua
Yu
Y
Jia-Ming
Yin
Y
Zhong-Wei
Yin
Y
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology*; D019328:Buthionine Sulfoximine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005978:Glutathione / Q000494:pharmacology*; D007672:Kidney Cortex / Q000187:drug effects; D007674:Kidney Diseases / Q000139:chemically induced* / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D008627:Mercuric Chloride / Q000037:antagonists & inhibitors / Q000633:toxicity; D008630:Mercury Poisoning / Q000188:drug therapy / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014494:Unithiol / Q000494:pharmacology
D000975:Antioxidants; D014494:Unithiol; D019328:Buthionine Sulfoximine; D008627:Mercuric Chloride; D005978:Glutathione; D001205:Ascorbic Acid