Toxicity of chronic ethanol ingestion and superoxide radical formation on seminal vesicles of rats
Food and Chemical Toxicology, ISSN: 0278-6915, Vol: 34, Issue: 10, Page: 1003-1007
1996
- 7Citations
- 2Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations7
- Citation Indexes7
- CrossRef5
- Captures2
- Readers2
Article Description
The toxic effects of chronic ethanol ingestion were evaluated in male adult rats for 300 days. The animals were divided into three groups: the controls received only tap water as liquid diet; the chronic ethanol ingestion group received only ethanol solution (30%) in semivoluntary research; and the withdrawal group received the same treatment as chronic ethanol-treated rats until 240 days, after which they reverted to drinking water. Chronic ethanol ingestion induced increased lipoperoxide levels and acid phosphatase activities in seminal vesicles. Cu-Zn superoxide dismutase (SOD) decreased from its basal level 70.8 ± 3.5 to 50.4± 1.6 U/mg protein at 60 days of chronic ethanol ingestion. As changes in GSH-PX activity were observed in rats after chronic ethanol ingestion, while SOD activities were decreased in these animals, it is assumed that superoxide anion elicits lipoperoxide formation and induces cell damage before being converted to hydrogen peroxide by SOD. Ethanol withdrawal induced increased SOD activity and reduced seminal vesicle damage, indicating that the toxic effects were reversible, since increased SOD activity was adequate to scavenge superoxide radical formation. Superoxide radical is an important intermediate in the toxicity of chronic ethanol ingestion.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0278691596000658; http://dx.doi.org/10.1016/s0278-6915(96)00065-8; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0030267909&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/9012776; https://linkinghub.elsevier.com/retrieve/pii/S0278691596000658; http://linkinghub.elsevier.com/retrieve/pii/S0278691596000658; http://api.elsevier.com/content/article/PII:S0278691596000658?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:S0278691596000658?httpAccept=text/plain; http://dx.doi.org/10.1016/s0278-6915%2896%2900065-8; https://dx.doi.org/10.1016/s0278-6915%2896%2900065-8
Elsevier BV
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