Effect of Selenium Supplementation on Serum Amylase, Lactate Dehydrogenase and Alkaline Phosphatase Activities in Rats Exposed to Cadmium or Lead

Şlencu, Bogdan Gabriel; Ciobanu, Constantin; Solcan, Carmen; Anton, Alina; Ciobanu, St.; Solcan, G.; Cuciureanu, Rodica

doi:10.1515/cerce-2015-0009

Cited by 7 publications

(6 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, the increased activities of ALT &AST in plasma clearly attributes to the leakage of these enzymes from the liver cytosol into the bloodstream. Earlier reports also suggested that lysosomal instability caused by Cd-toxicity resulted in the leakage of hepatic enzymes including ALT, AST and ALP into the blood stream [35]. In consonance with the above observations, there was a signi cant increased activity levels were recorded with AST & ALT, more over changes with ALT activities may also be attributed to the signi cant damage occurred during Cd-toxicity.…”

Section: Respiratory and Antioxidant Statussupporting

confidence: 77%

Amelioration of Cadmium-induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine

Poli

Madduru

Motireddy

2021

Preprint

View full text Add to dashboard Cite

The present study was performed to determine the protective effects of Vitamin C, Zinc and N-Acetylcysteine individually or in combinations with Cd, to monitor amelioration capability against Cd-induced oxidative damage in Wistar rats. Nine groups of rats were studied as experimental group. The present experiment was conducted for 45 days. Liver and kidneys were excised for biochemical determinations through assaying of antioxidant enzymes and lipid oxidation products to assess the impact of Cd-toxicity and its amelioration by co-administration of Vitamin C, Zinc and NAC along with Cd. Basal Metabolic rates, Tissue Respiration rates of liver and kidney were found to be significantly decreased (p < 0.05) during Cd toxicity. Serum biochemical parameters were also found to be significantly altered to cope up with Cd toxicity. All the antioxidant enzymes and products were significantly inhibited (p < 0.05) or elevated in rat liver and kidney tissues during Cd-induced toxicity. Whereas with co-administration of Vitamin C, Zinc and NAC, into rats clearly demonstrates the amelioration of oxidative damage induced by Cd-toxicity. From the results obtained in the present study all the agents tested had protective effects against Cd-induced oxidative damage.

show abstract

Section: Respiratory and Antioxidant Statussupporting

confidence: 77%

Amelioration of Cadmium-induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine

Poli

Madduru

Motireddy

2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Therefore, the increased activities of ALT and AST in plasma can be attributed to the leakage of these enzymes from the liver cytosol into the bloodstream. Earlier reports have suggested that lysosomal instability caused by Cd toxicity resulted in the leakage of hepatic enzymes, including ALT, AST and ALP into the blood stream [ 37 ]. Consonant with the above observations, there was a significant increased activity level recorded for AST and ALT; changes in ALT activities may also be attributed to the significant damage occurred during Cd toxicity.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Cadmium-Induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine

et al. 2022

View full text Add to dashboard Cite

The present study was performed to determine the protective effects of vitamin C, zinc, and N-acetylcysteine, individually or in combination with Cd, to monitor their amelioration capability against Cd-induced oxidative damage in Wistar rats. We investigated and demonstrated that cadmium is a toxic element that damages rat liver and kidney tissues. Vitamin C, zinc, and NAC have been proven to have protective roles against Cd toxic effects. Nine groups of rats were studied as the experimental group. The present experiment was conducted for 45 days. Liver and kidneys were excised for biochemical evaluation by assaying antioxidant enzymes and lipid oxidation products to assess the impact of Cd toxicity and its amelioration by co-administration of vitamin C, zinc, and NAC along with Cd. Basal metabolic rates and tissue respiration rates of liver and kidney were significantly decreased (p < 0.05) during Cd toxicity. Serum biochemical parameters were also found to be significantly altered to cope with Cd toxicity. All the antioxidant enzymes and products were significant inhibited (p < 0.05) or elevated in rat liver and kidney tissues during Cd-induced toxicity. Our results suggest that co-administration of vitamin C, zinc, and NAC to rats ameliorates oxidative damage induced by Cd toxicity. From the results obtained in the present study, all the agents tested had protective effects against Cd-induced oxidative damage.

show abstract

“…The increase in LDH level was observed during the chemical stress condition. [ 42 ] In this study, the administration of BPA significantly increased the LDH level, which might be due to the oxidative damage induced by the BPA in larvae. Recent studies have also reported that BPA increased the LDH level in rats.…”

Section: Discussionmentioning

confidence: 65%

Exposure to environmental pollutant bisphenol A causes oxidative damage and lipid accumulation in Zebrafish larvae: Protective role of WL15 peptide derived from cysteine and glycine‐rich protein 2

Guru

Arockiaraj

2022

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Humans are exposed to obesity causing Bisphenol A in various ways, especially through diet and food containers. Bioactive peptides are already reported to have antioxidant, antidiabetic, and antiobesity properties, which can mimic the role of mediators involved in obesity prevention. The protective effect of a short molecule or peptide, WL15 from cysteine and glycine‐rich protein 2 of a teleost of aquatic resource on Bisphenol A (BPA)‐induced lipid accumulation in zebrafish larvae was investigated. BPA exposure disrupted the antioxidant enzymes, apoptosis, and nitric oxide and led to changes in biochemical markers including alkaline phosphatase, lactate dehydrogenase, lipid peroxidation, glutathione S‐transferases, glutathione peroxidase, and reduced glutathione. However, WL15 inhibited the overproduction of oxidative stress, which correlates with its lipid‐lowering potential. BPA‐induced lipid accumulation in zebrafish showed an increase in triglyceride, cholesterol, and glucose level; simultaneously, WL15 treatment significantly reduced such accumulation in zebrafish. Evidenced by Oil red O staining and Nile red assay, WL15 inhibited lipid accumulation. At the same time, WL15 at 50 µM increases 2‐(N‐[7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl]amino)‐2‐deoxy‐d‐glucose (2NBDG) glucose uptake in zebrafish. In addition, gene expression studies in zebrafish larvae demonstrated that the WL15 peptide could play a crucial role in preventing lipid accumulation by downregulating the expression of lipogenesis‐specific genes. These results revealed an interesting and novel property of WL15, suggesting its potential application in preventing lipid accumulation through the hypolipidemic and antioxidant properties.

show abstract

Effect of Selenium Supplementation on Serum Amylase, Lactate Dehydrogenase and Alkaline Phosphatase Activities in Rats Exposed to Cadmium or Lead

Cited by 7 publications

References 24 publications

Amelioration of Cadmium-induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine

Amelioration of Cadmium-induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine

Amelioration of Cadmium-Induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine

Exposure to environmental pollutant bisphenol A causes oxidative damage and lipid accumulation in Zebrafish larvae: Protective role of WL15 peptide derived from cysteine and glycine‐rich protein 2

Contact Info

Product

Resources

About