scholarly journals Zinc Supplementation againstEimeria acervulina-Induced Oxidative Damage in Broiler Chickens

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Nedyalka V. Georgieva ◽  
Margarita Gabrashanska ◽  
Ventsislav Koinarski ◽  
Zvezdelina Yaneva

This study was undertaken to determine the dietary supplements of Zn containing diet on the antioxidant status in chickens experimentally infected withEimeria acervulina. The antioxidant status was monitored via determination of MDA concentrations and erythrocyte SOD and CAT activities, as well as vitamin E, vitamin C, Cu, and Zn in liver, muscle, and serum. The results showed increased MDA (), CAT (), and decreased SOD () in the infected birds. Significant changes in Cu and Zn concentrations and dramatically reduction of vitamin C and E concentrations in the infected chickens were found. The observed deviations in the studied enzymes and nonenzymatic parameters evidence the occurrence of oxidative stress following the infection and impaired antioxidant status of chickens, infected withEimeria acervulina. Our results proved the ameliorating role of CuZn(OH)3Cl (0.170 g per kg food) againstEimeria acervulina-induced oxidative damage in infected chickens.

Author(s):  
Amal Saad-Hussein ◽  
Gehan Moubarz ◽  
Sh. Abdalla Mohgah ◽  
Gh. Shousha Wafaa ◽  
H. Mohamed Aya

Abstract Background Aflatoxin B1 (AFB1) is classified as a Group I carcinogen. A Previous study found that oxidative stress from the metabolism of AFB1 induced hepatotoxic effects in wheat miller workers. Zinc and vitamin C may play a significant role in the activation of detoxification and overcoming the oxidative stress of AFB1. Objectives A prospective clinical trial was designed to evaluate the role of zinc and vitamin C oral supplementation on the oxidant-antioxidant status and the hepatotoxic effects of AFB1 in wheat miller workers. Methods Liver enzymes (ALT, AST, ALP, and GGT), P53 protein, malondialdehyde (MDA), glutathione S transferase (GST), Superoxide dismutase (SOD), zinc and vitamin C were estimated in 35 wheat miller workers before and after zinc and vitamin C supplementation for 1 month. Results The results revealed that zinc and vitamin C were significantly increased after the one-month supplementation, while liver enzymes (AST, ALP, and GGT), MDA, and GST of the workers were significantly decreased. SOD and P53 were also decreased but not to a significant level; SOD was decreased in 56% and P53 was decreased in 58% of the total workers. Conclusions Zinc and vitamin C oral supplementation for 1 month had an ameliorative effect on the hepatotoxicity of AFB1 in wheat miller workers, through decreasing MDA, SOD, and GST levels that in turn led to an improvement in their liver enzymes. Further study on a larger scale is needed to confirm these results.


2021 ◽  
pp. 117996
Author(s):  
Barbara Flasz ◽  
Marta Dziewięcka ◽  
Andrzej Kędziorski ◽  
Monika Tarnawska ◽  
Jan Augustyniak ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ken Shinmura

The biology of aging has not been fully clarified, but the free radical theory of aging is one of the strongest aging theories proposed to date. The free radical theory has been expanded to the oxidative stress theory, in which mitochondria play a central role in the development of the aging process because of their critical roles in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function associated with the accumulation of oxidative damage might be responsible, at least in part, for the decline in cardiac performance with age. In contrast, lifelong caloric restriction can attenuate functional decline with age, delay the onset of morbidity, and extend lifespan in various species. The effect of caloric restriction appears to be related to a reduction in cellular damage induced by reactive oxygen species. There is increasing evidence that sirtuins play an essential role in the reduction of mitochondrial oxidative stress during caloric restriction. We speculate that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally. Therefore, the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtuin biology into clinical practice.


2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Richard S Bruno ◽  
Yang Song ◽  
Scott W Leonard ◽  
Alan W Taylor ◽  
Maret G Traber ◽  
...  

Author(s):  
Ravi Ranjan Kumar ◽  
Lovekesh Singh ◽  
Amandeep Thakur ◽  
Shamsher Singh ◽  
Bhupinder Kumar

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity. Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript. Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain.


2018 ◽  
Vol 106 ◽  
pp. 232-238 ◽  
Author(s):  
Marija D. Milošević ◽  
Milica G. Paunović ◽  
Miloš M. Matić ◽  
Branka I. Ognjanović ◽  
Zorica S. Saičić
Keyword(s):  

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