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Hesperidin attenuates mitochondrial dysfunction during benzo(a)pyrene‐induced lung carcinogenesis in mice
Author(s) -
Kamaraj Sattu,
Anandakumar Pandi,
Jagan Sundaram,
Ramakrishnan Gopalakrishnan,
Devaki Thiruvengadam
Publication year - 2011
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2010.00812.x
Subject(s) - hesperidin , glutathione , glutathione reductase , benzo(a)pyrene , glutathione peroxidase , superoxide dismutase , biochemistry , chemistry , antioxidant , mitochondrion , vitamin e , malate dehydrogenase , lipid peroxidation , carcinogen , enzyme , medicine , pathology , alternative medicine
The present study is designed to assess the mitochondrial status during benzo(a)pyrene (B(a)P)‐induced lung carcinogenesis in Swiss albino mice and to reveal the modulatory effect of hesperidin over it. B(a)P (50 mg/kg body weight)‐induced mitochondrial abnormalities was evident from alterations in mitochondrial lipid peroxides, antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione‐S‐transferase, reduced glutathione, vitamin E, and vitamin C), major tricarboxylic acid (TCA) cycle enzyme activities (isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, alpha‐ketoglutarate dehydrogenase), electron transport chain (ETC) complexes activities and ATP levels. Ultrastructural changes in lung mitochondria were also in accord with the above aberrations. Hesperidin (25 mg/kg body weight) supplementation effectively counteracted all the above changes and restored cellular normalcy, indicating its protective role during B(a)P‐induced lung cancer.