The effects of beta glucan on toxicity induced lead in rats

Twenty-eight Sprague Dawley male rats were housed in individual cages and randomly divided into four groups; Control; Beta glucan (BG; 50 mg/kg body weight (BW)/day of BG, gavage; Lead (Lead; 15 mg/kg BW/day of lead acetate, ip), Lead + BG (Lead+ BG; 15 mg/kg BW/day of lead acetate, ip and 50 mg/kg BW/day of BG, gavage). Feed intake in the Lead+ BG group significantly increased in comparison with that of Lead group (P<0.001). Lead toxicity significantly increased MDA indicating oxidative stress. Beta glucan administration significantly decreased MDA levels, and increased the GSH-Px activity in the liver tissue (P<0.001). Lead administration increased expression of pro-apoptotic protein Bax, decreased the expression of the antiapoptotic protein Bcl-2 and increased ratio of Bax/Bcl-2 (P<0.01). It also impaired spermatogenesis (P<0.05). Treatment with Beta glucan on the Lead induced toxicity partially preserved suppressed oxidative stress, the activation of apoptotic pathways and spermatogenesis.