Coenzyme Q10 supplementation alleviates the oxidative stress on the liver imposed by mercuric chloride in albino rats
Benha Veterinary Medical Journal • 2023
معلومات البحث
المؤلفون
Aya Gamal, Mohamed Abo Salem, Elham Elshewy, Ahmed M. Hegazy, Samar S Ibrahim
الكلمات المفتاحية
Coenzyme Q10;HgCL2 ;Mercuric residues ;Oxidative stress
المجلة العلمية
Benha Veterinary Medical Journal
الناشر
Not Available
المجلد
43
العدد
2
الصفحات
19-24
publication.type
Local
رابط البحث
Open Link
المواد المرفقة
Not Available
الملخص
Mercury is given particular attention, because of its detrimental impacts on both human and animal health. It is claimed that it accumulates in the liver, causing liver toxicity and tissue
damage. Consequently, it was intended in the current research to explore the potential
antioxidant activity of coenzyme Q10 (CoQ10) against mercuric chloride (HgCl2)-induced
hepatotoxicity. Twenty-eight male albino rats were divided into four groups: control group;
given saline, CoQ10 group; given CoQ10 (10 mg/kg b.wt.); HgCl2 group; given mercuric
chloride (1 mg/kg b.wt.); and the co-treated group, given coenzyme Q10 (10 mg/kg b.wt.) plus
HgCl2 (1 mg/kg b.wt.). All treatments were received orally for 4 weeks. The HgCl2 group had
significantly higher serum concentrations of alanine aminotransferase, aspartate
aminotransferase, alkaline phosphatase, and lactate dehydrogenase enzymes, while total
protein and albumin values were significantly decreased. Rats also showed a significant
increase in mercury concentration and exhibited a notable spike of lipid peroxidation levels
with concurrent declines in antioxidant enzyme (GSH). This result was concomitant with
histopathological changes of examined liver tissues. Treatment with Co-treatment with CoQ10
ameliorated the hepatotoxicity induced by HgCl2 as indicated by improved serum biochemical
parameters, oxidative markers, histopathological features of hepatic tissues. In conclusion,
CoQ10 could be the best choice to counteract the liver toxicity produced by mercuric chloride
exposure through its antioxidant effect.
damage. Consequently, it was intended in the current research to explore the potential
antioxidant activity of coenzyme Q10 (CoQ10) against mercuric chloride (HgCl2)-induced
hepatotoxicity. Twenty-eight male albino rats were divided into four groups: control group;
given saline, CoQ10 group; given CoQ10 (10 mg/kg b.wt.); HgCl2 group; given mercuric
chloride (1 mg/kg b.wt.); and the co-treated group, given coenzyme Q10 (10 mg/kg b.wt.) plus
HgCl2 (1 mg/kg b.wt.). All treatments were received orally for 4 weeks. The HgCl2 group had
significantly higher serum concentrations of alanine aminotransferase, aspartate
aminotransferase, alkaline phosphatase, and lactate dehydrogenase enzymes, while total
protein and albumin values were significantly decreased. Rats also showed a significant
increase in mercury concentration and exhibited a notable spike of lipid peroxidation levels
with concurrent declines in antioxidant enzyme (GSH). This result was concomitant with
histopathological changes of examined liver tissues. Treatment with Co-treatment with CoQ10
ameliorated the hepatotoxicity induced by HgCl2 as indicated by improved serum biochemical
parameters, oxidative markers, histopathological features of hepatic tissues. In conclusion,
CoQ10 could be the best choice to counteract the liver toxicity produced by mercuric chloride
exposure through its antioxidant effect.
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