Protective role of zinc in nickel induced hepatotoxicity in rats

Sidhu, Pardeep; Garg, M. L.; Dhawan, D. K.

doi:10.1016/j.cbi.2004.09.012

Cited by 83 publications

(47 citation statements)

References 36 publications

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“…The decreased body weight is concomitant with previously reports [29]. This reduction in weights might as a result of the overall increased degeneration of lipids and proteins [30]. Findings indicated also an increase of absolute and relative kidney weights, which might be explained by the hypertrophy and the selective accumulation of nickel in the kidney [26,31].…”

Section: Discussionsupporting

confidence: 71%

Effect of Silymarin Extracted From Silybum Marianum on Nickel Hematotoxicity and Nephrotoxicity in Male Albino Wistar Rats

Bouhalit

Kechrid

Elfeki

2017

Int J Pharm Pharm Sci

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Objective: The objective of this study was to investigate the effect of silymarin extract from Silybum marianum against nickel-induced alterations in haematological indices, kidney dysfunction and renal antioxidant defence system. Methods:Male albino Wistar rats were divided into four groups seven each. Control, silymarin, nickel and nickel plus silymarin. Silymarin was administrated orally (100 mg/kg b. wt) and nickel as nickel sulfate (NiSO4 6H2 Results:The treatment with nickel led to a significant decrease in body weight with an increase in both absolute and relative kidney weights and a significant increase in renal markers, which confirmed by histopathological alteration. A microcytic anemia was also observed, which was manifested by a reduction of red blood cells count (RBC), hemoglobin (Hb) concentration, platelet counts (Plt), hematocrit and white blood cells counts (WBC). The level of lipid peroxidation was increased. Whereas, GSH concentration and enzymatic antioxidants SOD, GSH-Px and CAT activities were decreased. The co-treatment with methanolic extract of milk thistle attenuated the variation in the hematological and renal markers, decreasing renal lipid peroxidation (p<0.05) with a concomitant increasing reduced glutathione content (p<0.01) and restoring the antioxidant enzymes (SOD, CAT, GSH-Px) in kidney, as well as an improvement in histological changes compared to those previously noticed in nickel group. 0) was given intraperitoneally (20 mg/kg b. wt) at alternative days. The experiment continued for three consecutive weeks. Body weight was recorded regularly. After overnight fasting, animals were killed and serum creatinine, serum urea, serum uric acid, hematological parameters and renal antioxidant markers were determined. Conclusion:To conclude, these findings demonstrated that silymarin extract effectively improved heamatotoxicity and nephrotoxicity caused by nickel.

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Section: Discussionsupporting

confidence: 71%

Effect of Silymarin Extracted From Silybum Marianum on Nickel Hematotoxicity and Nephrotoxicity in Male Albino Wistar Rats

Bouhalit

Kechrid

Elfeki

2017

Int J Pharm Pharm Sci

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“…Further, zinc functions as a complex antioxidant. It participates in superoxide dismutase and other enzymatic activities, stabilizes cell membranes, and inhibits lipid peroxidation (Smart, 1992); the same has already been reported in our earlier studies (Sidhu et al, 2006;Sidhu et al, 2005;Sidhu et al, 2004). Inhibiting lipid peroxidation can further stabilize the membrane fluidity and, thus, regulate the activity of acetylcholinesterase.…”

Section: Discussionsupporting

confidence: 51%

Effectiveness of Zinc in Modulating Lithium Induced Biochemical and Behavioral Changes in Rat Brain

2007

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1. The purpose of the present study was to determine the effect of zinc on the status of various neurotransmitters as well as behavioral patterns of lithium-treated rats. The study was designed with a view to find out whether zinc affords protection to brain against lithium toxicity. 2. Animals were segregated into four different groups. Animals in group I were fed with standard laboratory feed and water ad libitum and served as normal controls. Animals in group II and IV were given lithium in the form of lithium carbonate in their diet at a dose level of 1.1 g/Kg diet. Animals in group III and IV were given zinc treatment in the form of zinc sulfate at a dose level of 227 mg/L mixed in drinking water of animals. 3. The effects of all the treatments were studied for a duration of 1, 2, and 4 months with regard to the parameters, which included estimation of serotonin and dopamine concentrations as well as the activity of acetylcholinesterase in cerebral cortex of rat brain. Further, passive avoidance, active avoidance, and behavior despair tests were conducted to assess the short-term memory, cognitive behavior, and psychomotor dysfunction of the animals, respectively. 4. Initially, a decrease in the acetylcholinesterase activity was reported in cerebral cortex followed by an increase in the enzyme activity after 2 and 4 months of lithium treatment. Serotonin concentration significantly decreased after 2 and 4 months of lithium treatment, whereas dopamine concentration increased significantly after 4 months of lithium treatment. Zinc administration to the lithium-treated group significantly improved the acetylcholinesterase activity as well as the concentration of dopamine and serotonin. Further, lithium-treated rats showed an increase in depression time as compared to normal controls both after 1 and 4 months of treatment. Short-term memory significantly improved in lithium-treated rats in all treatment groups. However, no change in the cognitive behavior of the animals was reported after lithium treatment. Zinc co-administration with lithium significantly improved the short-term memory and cognitive functions of the animals. From the above results it can be concluded that zinc proved beneficial in altering the status of neurotransmitters as well as the behavior patters of the animals treated with both short and long-term lithium therapy.

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“…Thus, the expression of Mt-1/2 ultimately improves survival in the progression of nickel-induced acute lung injury in mice. The induction of Mt-1/2 also protected rat liver from the toxic effects of nickel following acute exposure [61]. However, Mt-1/2 overexpression did not prevent nickel-induced tumor formation in mice that received intramuscular injections of nickel [62,63].…”

Section: Genes Coding For Metal-binding Proteinsmentioning

confidence: 96%

“…Nickel treatment also resulted in a signifi cant increase in lipid peroxidation and enzymatic activities of catalase and glutathione-S-transferase in vivo [61,157]. High levels of alanine aminotranferase and aspartate aminotransferase were found in serum of exposed animals.…”

Section: Nickel-induced Oxidative Stressmentioning

confidence: 99%