Chronic nasal instillation of residual-oil fly ash (ROFA) induces brain lipid peroxidation and behavioral changes in rats.
Several epidemiological studies have linked particulate matter exposure to numerous adverse health effects on the respiratory, cardiovascular, and reproductive systems (Braga et al., 1999; Zanobetti et al., 2000; Anderson et al., 2001; Farhat et al., 2005). More recently, ambient levels of black carbon were associated to impaired cognitive function in children (Suglia et al., 2008), suggesting that the central nervous system (CNS) may be a target of air pollutants. The present study was conducted to (a) determine whether chronic residual oil fly ash (ROFA) exposure promotes behavioral changes and lipid peroxidation in rat brain areas, and (b) determine whether N-acetylcysteine (NAC), a general antioxidant, prevents these effects. Forty-five-day-old male Wistar rats were exposed or not to ROFA by intranasal instillation and were treated or not with NAC (150 mg/kg) ip for 30 days. One day later, rats were submitted to the open field test to evaluate the motor/exploratory activities and emotionality followed by decapitation. Striatum and cerebellum were dissected to determine lipid peroxidation by the accumulation of thiobarbituric acid-reactive substances (TBARS). ROFA instillation induced an increase in lipid peroxidation level in striatum (p = .033) and cerebellum (p = .030), as compared with the control group. NAC treatment blocked these changes. ROFA promoted a decrease in the frequency of peripheral walking (p = .006) and a decrease in exploration (p = .001), which were not blocked by N-acetylcysteine. The present study provides evidence that toxic particles, administered by the respiratory route, induce oxidative stress in structures of the central nervous system, as well as behavioral alterations. The administration of NAC reduces lipid peroxidation at the striatum and cerebellum levels, but does not influence behavioral disturbances.
Zanchi
Ana Claudia
AC
Post-Graduation Course in Medical Sciences and Laboratory of Oxidative Stress and Atmospheric Pollution, Fundação Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, Brazil.
Venturini
Carina Duarte
CD
Saiki
Mitiko
M
Nascimento Saldiva
Paulo Hilario
PH
Tannhauser Barros
Helena Maria
HM
Rhoden
Claudia Ramos
CR
D000111:Acetylcysteine / Q000494:pharmacology; D000281:Administration, Intranasal; D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002244:Carbon / Q000633:toxicity*; D060729:Coal Ash; D004195:Disease Models, Animal; D005106:Exploratory Behavior / Q000187:drug effects; D016166:Free Radical Scavengers / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D052638:Particulate Matter / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000393:Air Pollutants; D060729:Coal Ash; D016166:Free Radical Scavengers; D052638:Particulate Matter; D017392:Thiobarbituric Acid Reactive Substances; D002244:Carbon; D000111:Acetylcysteine