Deleterious Effect of Abamectin on Rat Brain Mitochondria

Reda K. Abdel-Razik and Nadia A. Hamed

The neurological damages resulted by abamectin (ABA) poisoning is not completely elucidated, especially in cellular organelles such as mitochondria. In the present study, the pro-oxidant effect of ABA on rat brain mitochondria was first investigated. A single oral dose of ABA (3.3mg / Kg body weight; 1/3 LD50) was given to rat and the brain mitochondria were isolated at various times (4, 24 and 336 h) after dosing. Oxidative stress in this organelle was noticed, since it provokes a significant reduction in the activity of adenosine triphosphatase (ATPase) and superoxide dismutase (SOD) and reduced glutathione (GSH) level. In addition, a significant increase in malondialdehyde (MDA) level was observed in neuronal mitochondria, indicating clearly an intense peroxidation within mitochondria. Second, the histochemical evaluation was carried out to estimate the extent of ischemic brain injury as a result of ABA exposure. The average area of infarct for the neurologically impaired rats was increased in a time-dependent manner. The percentage of surface area of each infarcted section was found to correlate with the severity of the neurologic deficit. The results suggest that ABA-induced neuronal mitochondrial toxicity may be an important contributing factor to brain aging and neurodegenerative diseases.