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DOI 10.1179/1351000214y.0000000101

Медицинская библиотека · Redox report : communications in free radical research · 2014

Oxidative stress and antioxidant status in patients with autoimmune liver diseases.

Kaffe Eleanna T, Rigopoulou Eirini I, Koukoulis George K, Dalekos George N, Moulas Anargyros N

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

OBJECTIVE

To estimate oxidative stress and antioxidant components during different stages of autoimmune liver diseases and assess their possible implication on disease progression.

METHODS

We determined several markers of oxidative injury (isoprostane, aldehydes, protein carbonyls, 3-nitrotyrosine, and myeloperoxidase) and antioxidant components (glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase) in whole blood, serum, and urine in 49 patients with autoimmune cholestatic liver diseases (AC) and 36 patients with autoimmune hepatitis (AIH) and healthy subjects matched for sex and age.

RESULTS

Both AC and AIH patients had increased levels of all lipid and protein oxidative injury products and significantly decreased whole blood glutathione levels compared to controls. AIH patients had significantly higher levels of aldehydes and glutathione peroxidase activity and significantly lower protein carbonyl levels compared to AC patients. Protein carbonyl and isoprostane levels increased and glutathione levels decreased gradually with progression from mild fibrosis to severe fibrosis and cirrhosis in both AC and AIH patients. In addition, both cirrhotic AC and AIH patients had significantly higher protein carbonyls compared to non-cirrhotics.

DISCUSSION: We provide novel findings in support of a major contribution of oxidant/antioxidant imbalance in the progression of liver injury in AC and AIH.

Для цитирования: Kaffe Eleanna T, Rigopoulou Eirini I, Koukoulis George K, Dalekos George N, Moulas Anargyros N. Oxidative stress and antioxidant status in patients with autoimmune liver diseases.. Redox report : communications in free radical research. 2014. DOI: 10.1179/1351000214y.0000000101.

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