Short term sublethal studies in rats exposed to nickel subsulfide and nickel ore : effects on oxidative damage, antioxidant and detoxicating enzymes

Chang, Xiangning (2000) Short term sublethal studies in rats exposed to nickel subsulfide and nickel ore : effects on oxidative damage, antioxidant and detoxicating enzymes. Masters thesis, Memorial University of Newfoundland.

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Abstract

Nickel is a ubiquitous trace metal which occurs in soil, water, air, and in the biosphere. Some nickel compounds have been shown to induce tumor at injection site in animals. Lung and nasal cancers have been observed in workers at nickel refineries. The mining of nickel in Voisey's Bay may possibly pose risks of environmental concern, especially to aquatic species. The sublethal effects of nickel subsulfide and nickel ore with respect to oxidative damage, antioxidant and detoxicating enzymes were examined in short term studies in rats. -- The rats were given nickel subsulfide (100 mg/rat or 200 mg/rat), i.p., as a single dose or two doses, 2 weeks prior to sacrifice. Nickel subsulfide suppressed catalase and superoxide dismutase (SOD) activities in rat liver but not in kidney. The inhibition in hepatic SOD showed a dose-dependent relationship. The decrease of hepatic catalase and SOD by nickel subsulfide could be a reflection of nickel insult which could make target tissues more vulnerable under oxidative stress. -- Other groups of rats were given nickel ore (100, 200 mg/rat), i.p., as a single dose, two days, one week or two weeks prior to sacrifice. Nickel ore treatment did not affect lipid peroxidation, protein carbonyi content, aminolevulinic dehydratase, catalase, superoxide dismutase, glutathione peroxidase, glutathione levels, glutathione reductase, glutathione S- transferase (l-nitro-2,4-dichlorobenzene, ethacrynic acid, trans-4-phenyi-3-buten-3-one) in rat liver or kidney to any significant extent. A statistically significant increase was observed in liver NAD(P)H: quinone reductase activity in the group treated with 200 mg/rat (2 w); the enhancement rate averaged 117%. An significant increase also occurred in kidney glutathione S-transferase (l-chloro-2,4-dinitrobenzene) activity in the groups treated with 100, 200 mg/rat (2 d) and this activation seemed to be induced in a dose-dependent manner. It appears that nickel ore does not pose a serious toxic insult to rats in short term studies and hence the risk posed to aquatic species could be minor. However, long-term studies with rainbow trout and bivalves need to be conducted to investigate possible risks of more broadscale environmental concern.

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