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CARBARYL EFFECTS ON OXIDATIVE STRESS IN BRAIN REGIONS OF ADOLESCENT AND SENESCENT BROWN NORWAY RATS
Citation:
KODAVANTI, PRASADA RAO S., J. E. ROYLAND, J. Richards, AND R. C. MACPHAIL. CARBARYL EFFECTS ON OXIDATIVE STRESS IN BRAIN REGIONS OF ADOLESCENT AND SENESCENT BROWN NORWAY RATS. Presented at Society of Toxicology (SOT) Annual Meeting, San Francisco, CA, March 11 - 15, 2012.
Impact/Purpose:
This study explored Oxidative Stress (OS) as as a potential toxicity pathway for carbaryl exposure (a carbamate insecticide) and whether these effects were age-dependent.
Description:
Oxidative stress (OS) plays an important role in susceptibility and disease in old age. Understanding age-related susceptibility is crucial in assessing the human health risks of chemicals. Growing evidence implicates as in carbamate toxicity in addition to cholinesterase-inhibiting effects. This study explored OS as as a potential toxicity pathway for carbaryl exposure (a carbamate insecticide) and whether these effects were age-dependent. OS-related events included reactive oxygen species production [NADPH Quinone oxidoreductase 1 (NQO 1), NADH Ubiquinone reductase (UBIQ)], antioxidant homeostasis [total antioxidant substances (TAS)], and oxidative DNA damage (total aconitase). Male Brown Norway rats (l and 24 months) were dosed orally with carbaryl (0, 7.5 or 15 mg/kg) in corn oil. Frontal cortex (FC), cerebellum (CB), striatum (ST), and hippocampus (HP) were dissected 2 hours after exposure, quick frozen, and stored at -80°C until analysis. Results indicated substantial age-related increases in ROS production (~6x in UBIQ-RD and > 8x in NQO1), decreases in antioxidant homeostatic mechanisms (i.e, TAS ~2x), and decrease in aconitase activity (2-3 x) regardless of brain area. The effects of carbaryl treatment were age-and brain area-specific. In general, effects on as parameters were greater at 1 mo vs. 24 mo. Interestingly, measures of ROS production were often in opposition to each other (e.g. UBIQ-RD decreased ~26% in the striatum at 1 mo of age while NQOl was increased ~26%) possibly indicating activation of different compensatory pathways. Carbaryl generally decreased or had no effect on TAS. Also similar to the age effect, aconitase levels were decreased by carbaryl in some brain regions. These results indicate as as a potential toxicity pathway, but the complex interaction between age and carbaryl exposure on as parameters in different brain regions require further investigation. (This abstract does not necessarily reflect USEPA policy).