3.8 Article

Role of Co Q-10 in Copper Sulphate Toxicity in Chick's Model

Journal

EGYPTIAN JOURNAL OF VETERINARY SCIENCE
Volume 53, Issue 3, Pages 431-441

Publisher

NATL INFORMATION DOCUMENTATION CENTRE
DOI: 10.21608/EJVS.2022.139810.1343

Keywords

Coenzyme Q-10; Copper Sulfate; Oxidative stress; Caspase-3; Chicks

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The study demonstrated that coenzyme Q-10 could counteract the damage caused by copper sulphate poisoning, reduce oxidative stress, and alleviate histopathological changes in the brain.
OUR aim was to investigate the ability of coenzyme Q-10 to counteract the damage caused by copper sulphate poisoning, at the nervous system pharmacological challenge levels, oxidative stress and, some biochemical parameters, as well as study of histopathological changes in the brain. In this experiment, 72 chicks were randomly divided into 6 groups of 12 chicks each. Only distilled water was administered to the G1 control group. Copper sulphate alone at a dose of 19.5 mg/kg was given to the G2 group. The G3 group was given 30 mg/kg of CO Q-10 alone for 7 days. The G4 group was given copper sulphate for 3 days and Q-10 for 7 days. The G5 group was given copper sulphate for 3 days before receiving CoQ-10 for 7 days. The G6 group was given coenzyme Q-10 alone for 7 days before being given copper sulphate for 3 days. The pharmacological challenge revealed substantial differences in the onset of sleep and sleep duration in chicks given co-enzyme Q-10 with copper sulphate at various times. Total oxidative stress, glutathione, and malondialdehyde in serum and brain tissue were also linked to an increase in Caspase-3 activity in brain tissue, while groups that received coenzyme Q-10 with copper sulphate concurrently or prior to oxidative stress had less oxidative stress and less histopathological changes in brain tissue. We concluded that giving the Co Q-10 at the same time as or before copper sulphate lowered the toxicity of copper sulphate. Some oxidative stress markers, as well as biochemical indicators, histopathological abnormalities, and programmed cell death in brain cells, were used to demonstrate this.

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