Controlled ozone (O(3)) administration is known to promote oxidative preconditioning and, thus, may reverse chronic oxidative stress that accompanies aging. Therefore, the present work was undertaken to study the potential role of O(3) in ameliorating certain age-related biochemical changes represented by impaired activities of inner mitochondrial membrane enzymes, compromised energy production and increased oxidative burden in male rat cerebral cortex. Prophylactic administration of O(3)-O(2) mixture to 3 month-old rats, at an intrarectal dose of 0.6 mg O(3) kg(-1) body weight twice/week for 3 months then once/week until the age of 15 months, normalized reduced glutathione content, adenosine triphosphate/adenosine diphosphate ratio, mitochondrial superoxide dismutase (SOD) and complex IV (cytochrome-c oxidase) activities, improved glutathione redox index (GSHRI), complex I (NADH-ubiquinone oxidoreductase) and mitochondrial nitric oxide synthase (mtNOS) activities, and attenuated the rise in malondialdehyde (MDA) and mitochondrial protein carbonyl levels. On the other hand, therapeutic administration of the same dose of O(3)-O(2) mixture to 14 month-old rats three times/week for 1 month, reduced mitochondrial protein carbonyl level only. Other favorable effects, including normalization of Na,K-adenosine triphosphatase (Na,K-ATPase) activity and reduction in lipofuscin level in the prophylactic group, as well as improvement in mitochondrial SOD and complex I activities with a decrease in total MDA level in the therapeutic group, were comparable to the effects observed in the corresponding O(2)-treated control groups. In conclusion, the present study revealed that prophylactic administration of O(3)-O(2) mixture provided better amelioration of age-related cerebrocortical alterations by combining the advantages of both O(3) and O(2) therapies.
The effects of benzo[a]pyrene (B[a]P) on some drug-metabolizing and antioxidant systems in liver, lung, and stomach were investigated in normal and protein malnutrition (PM) rats. PM significantly inhibited tissue glutathione (GSH) content and increased hepatic lipid peroxidation. Cytochrome P450 isoform CYP1A1 was significantly increased in various tissues (42-73%). Also, lung glutathione S-transferase (GST) activity was significantly decreased (19%) in PM rats. On the other hand, B[a]P significantly induced tissue GSH of control and PM rats. Also, hepatic lipid peroxidation were significantly increased in control rats treated with B[a]P. Superoxide dismutase (SOD) activity was decreased by B[a]P treatment in PM rat stomach. B[a]P significantly induced both quinone reductase (QR) (in all tissues) and hepatic GST of control and PM rats. GST activity in PM rat liver was significantly higher than that of control rat liver after B[a]P treatment. Also, B[a]P induced hepatic CYP1A1 by 32-fold and 27-fold (P < or = 0.05) in control and PM rats, respectively. Stomach and hepatic UDP-glucuronosyltransferase activities were significantly decreased (34%) and increased (74%), respectively by B[a]P in PM rats. The results suggest that PM status has a modifying effect on the response of some antioxidant and metabolizing systems to a well-known carcinogen risk.
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