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Life‐long supplementation with a low dosage of coenzyme Q 10 in the rat: Effects on antioxidant status and DNA damage
Author(s) -
Quiles José L.,
Ochoa Julio J.,
Battino Maurizio,
GutierrezRios PurificaciÓN,
Nepomuceno Eduardo A.,
Frías Magdalena LÓPez,
Huertas Jesús R.,
Mataix JosÉ
Publication year - 2005
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520250109
Subject(s) - antioxidant , coenzyme q10 , polyunsaturated fatty acid , tocopherol , medicine , dna damage , antioxidant capacity , endocrinology , retinol , chemistry , coenzyme q – cytochrome c reductase , vitamin e , biochemistry , dna , biology , vitamin , fatty acid , cytochrome c , mitochondrion
Life‐long low‐dosage supplementation of coenzyme Q 10 (CoQ 10 ) is studied in relation to the antioxidant status and DNA damage. Thirty‐two male rats were assigned into two experimental groups differing in the supplementation or not with 0.7 mg/kg/day of CoQ 10 . Eight rats per group were killed at 6 and 24 months. Plasma retinol, α‐tocopherol, coenzyme Q, total antioxidant capacity and fatty acids were analysed. DNA strand breaks were studied in peripheral blood lymphocytes. Aging and supplementation led to significantly higher values for CoQ homologues, retinol and α‐tocopherol. No difference in total antioxidant capacity was detected at 6 months but significantly lower values were found in aged control animals. Similar DNA strand breaks levels were found at 6 months. Aging led to significantly higher DNA strand breaks levels in both groups but animals supplemented with CoQ 10 led to a significantly lower increase in that marker. Aged rats showed significantly higher polyunsaturated fatty acids. This study demonstrates that lifelong intake of a low dosage of CoQ 10 enhances plasma levels of CoQQ 9 , CoQ 10 , α‐tocopherol and retinol. In addition, CoQ 10 supplementation attenuates the age‐related fall in total antioxidant capacity of plasma and the increase in DNA damage in peripheral blood lymphocytes.