P-207: Deltamethrin-Induced Derangements Correlates with Estrogen Synthesis, Angiogenesis and Oxidative Stress

Background: Deltamethrin (DTM) is a pyrethroid derivative, which is the most potent products of Type 2 insecticides and acts by delaying the closure of sodium channels. Estrogen as a vascular growth factor on ovarian tissue plays an essential impact further to its involvement in follicular growth. On the other hand, the role of angiogenesis on ovarian tissue in inhibiting the apoptotic provokers has been reported previously. Impaired angiogenesis results in severe oxidative stress, which in turn enhances the cellular DNA and RNA damages. Therefore, current study was performed in order to evaluate the effect of DTM on estrogen synthesis and uncover the correlation between estrogendependent impaired angiogenesis and follicular atresia. Materials and Methods: Twenty four mature virgin female Wistar rats were assigned into four groups as; control-sham group (received 0.5mL corn oil), 1mg/kg-1 DTM-administrated, 3mg/ kg-1 DTM-treated and 7mg/kg-1 DTM-received groups. All animals received the chemicals orally by gavages for 14 days. The angiogenesis and RNA damage were evaluated by using CD31+ immunohistochemical and Bickis epi-fluorescent techniques, respectively. The tissue levels of GSH-px, SOD, TTM and TAC, and serum level of estrogen were assessed. Moreover, the total and atretic follicles were counted per ovary. Results: DTM significantly (p<0.05) reduced angiogenesis and declined tissue GSH-px, SOD, TTM and TAC levels. The DTM-treated animals exhibited severe RNA damage and considerably enhanced follicular atresia. Serum level of estrogen decreased dose dependently. Conclusion: DTM by reducing estrogen synthesis resulted in impaired angiogenesis that partly enhanced oxidative stress via downregulating antioxidant capacity. Produced oxidative stress promoted the RNA damage and ultimately resulted in severe follicular atresia.