ABSTRACT
Deltamethrin is a synthetic pyrethroid insecticide used extensively to increase crop production. Regular exercise can help to protect from chronic disorders including chronic cardiovascular diseases and diabetes mellitus. The present study was designed to investigate the effect of deltamethrin [DM] on the induction of diabetes using streptozotocin [STZ] as an experimental model in normal and exercise trained adult male Sprague-Dawely rats. Also, to study the effects of exercise training on the oxidative stress induced by DM and diabetes. One hundred male Sprague-Dawley male rats were divided into two main groups normal and exercise trained [ET] groups. Exercise training was conducted by allowing animals to swim freely in swimming pool 15mm daily for 30 days. Animals of each main group were subdivided into control, corn oil, streptozitocin [STZ], deltamethrin [DM] and strep to zitocin+deltamethrin [ST2+DM] groups. Streptozetocin was given once by I.P. [40 mg/kg body weight in citrate buffer] and deltamethrin was administered orally [14 mg/kg] for 30 days. At the end of the experiment blood samples were withdrawn from the retro-orbital plexus for the estimation of serum glucose and serum insulin levels. And animals were euthanized and livers were removed for measuring the enzymatic and non-enzymatic oxidative stress biomarkers. The results explored that exercise training caused elevation in glucose level. DM caused a decrease in glucose level in exercise trained rats. Glucose level in STZ treated groups was increase by 4 folds relative to control effect, while STZ ET rats increased glucose level 3 folds than ET rats. Also, [SIZ+DM] in normal and ET rats caused increase in glucose level as compared to corresponding control. Training caused reduction in insulin level. Also, Serum insulin level was significantly decreased in normal untrained deltamethrin treated rats while its levels did not change [more or less] in trained groups. In addition, ST2 and [ST2+DM] in normal and ET rats reduced insulin level. Level of reduced glutathione [GSH] was dramatically increased in ET rats relative to normal untrained rats and their levels were decreased in DM, ST2 in normal and ET rats and [STZ+DM] ET rats. To the contrary, [STZ+DM] showed dramatic increase in GSH level in normal untrained rats. Lipid peroxidation [MDA] was enhanced in ET rats, DM El rats and ST2 ET rats compared to corresponding control. On the other hand, MDA severely increased its level both in normal untrained DM and ST2 either alone or in combination. Super oxide dismutase enzyme [SOD] activity was severely decreased by exercise. Its activity was also decreased in STZ, DM and [STZ+DM] untrained groups while it was increased in trained groups. Catalase enzyme [CAT] activity was also decreased in STZ, DM and [STZ+DM] normal and ET groups. Also, ET caused reduction in CAT activity as compared to control untrained rats. The results explored that both of DM and STZ alone or in combination administered to normal untrained rats did not change the protein content o liver. To the contrary, the protein content showed a significant decrease in the exercise trained groups [DM, ST2+DM] and significant increase in ST2 treated animals. Also ET rats showed increase in total protein level as compared to untrained rats. So we concluded that DM potentiates the effects of ST2 in the diabetic rats. Training improves diabetic state. Training partially improves antioxidant state by increasing antioxidant content of GSH and increasing SOD activity but it still fails to improve the damage caused by ST2 and or DM under our experimental conditions