Could an acute exposure to arsenite induce oxidative stress in rat brain?

ROBELLO E; BONETTO J; NAVONI J; VILLAAMIL E; PUNTARULO S

Ciudad Autónoma de Buenos Aires

Congreso; VIII Meeting of the Society for Free Radical Biology and Medicine-South American Group; 2013

Society for Free Radical Biology and Medicine, South American Group

Arsenic is known to produce a multi-systemic injury. However, little is known about arsenic-induced brain damages. Even though, oxidative stress is currently accepted as a factor in arsenic toxicity, the involved mechanism(s) has not been fully described. Adult male Wistar rats were treated with a single dose i.p. of sodium arsenite (5.8 mg/ arsenic/kg b.w.). Samples of whole brain and blood were taken at 0, 4, 8, 16, 24 and 31 h post treatment. Total arsenic content was determined by HG-AAS. Ascorbyl (Asc) and ascorbate (AH-) was determined by HPLC-EQ. Hydroxyl radical (OH) was determined by EPR in brain samples. Significant increase of arsenic in blood and brain was observed after 24 h. Neither the ascorbyl (Asc)/ascorbate (AH-) ratio nor the rate of generation of hydroxyl radical (OH), presented significant differences between controls and treated animals at this time. These results indicate that oxidative stress conditions have not been developed at the hydrophilic cellular environment. However, further experiments are required to assess a possible triggering of oxidative stress in the lipophilic medium.