Repeated endosulfan exposure induces changes in neurochemicals, decreases ATPase transmembrane ionic-pumps, and increased oxidative/ nitrosative stress in the brains of rats: Reversal by quercetin
Neurochemical and ATPase deregulations play important role in toxicant-induced neurodegeneration. Previous
studies have shown that loss of ATPase ionic-pumps alters neurochemical balance via increased ammonia,
oxidative and nitrosative stress. Thus, this study investigated the ameliorative potentials of quercetin on
neurochemical, ATPase changes, hyperammonemia and oxidative/nitrosative status in the brains of Wistar rats
exposed to endosulfan, a known toxic environmental pesticide that is casually used in many developing countries.
Adult rats were divided into five treatment groups (n = 5). Groups 1–2 received normal saline and corn oil
(vehicle) (10 mL/kg/day), group 3 received quercetin (20 mg/kg/day) orally for 28 days consecutively. However,
animals in groups 4–5 were given endosulfan (5 mg/kg/day, p.o) for 28 days. But, from the 14th to 28th
day, group 4 additionally received vehicle (10 mL/kg/day, p.o.), while group 5 was treated with quercetin (20
mg/kg/day, p.o.). Thereafter, brain levels of neurochemicals, ATPase activities, ammonia and oxidative/nitrosative
stress were investigated by employing standardized biochemical assay protocols. Quercetin increased
endosulfan-induced decreased levels of norepinephrine, dopamine, GABA, and decreased elevated concentrations
of glutamate and serotonin. Quercetin normalized the increased levels of acetylcholinesterase and
ammonia. Furthermore, quercetin significantly reversed the decrease in Na /K , Ca2 , Mg2 -ATPase activities
induced by endosulfan. Also, quercetin increased superoxide dismutase, catalase and glutathione peroxidase
activities, and reduced nitrite and peroxynitrite levels in brains of rats. These findings further provide evidence of
the ameliorative potential of quercetin against endosulfan-induced neurotoxicity via attenuation of neurochemical,
ATPase changes, and inhibition of acetylcholinesterase activity, ammonia release and oxidative/
nitrosative stress in rat brains.
Authors Name: Mega O. Oyovwi a, Benneth Ben-Azu b,*, Edesiri P. Tesi c, Abioye A. Oyeleke a, Christian I. Uruaka d, Rotu A. Rotu e, Eneni Okubo Aya-Ebi f
Email: tesi.edesiri@mydspg.edu.ng