The Effect of Ascorbic Acid and Garlic Administration on Lead-Induced Apoptosis in Rat Offspring's Eye Retina

Introduction: Lead toxicity induces retinal cell apoptosis. Vitamin C and garlic may decrease lead-induced apoptosis. This study was undertaken to investigate vitamin C and garlic protective effects on lead-induced apoptosis in eye retina. Methods: Pregnant Wistar rats (n = 72) were divided randomly into 9 groups: (L) treated rats with lead acetate in drinking water and (L+AA) with leaded water and vitamin C intraperitoneally;(L+G), the rats received leaded-water and garlic juice via gavage; (L+AA+G) treated rats with leaded water, ascorbic acid, and garlic juice, (AA) with ascorbic acid, and (G) with garlic juice; (AA+G) treated rats with vitamin C and garlic juice and (Sh) with tap water plus normal hydrogen chloride (HCl) and glucose; normal (N). After 21-day lactation, blood lead level (BLL) in rats was measured, and then their offspring and the rat offspring''s eyes were removed and processed for using TUNEL method. TUNEL positive cells in the eye retina were counted and all groups were compared. Results: BLL increased in L group compared to the control groups and decreased significantly in L + G, L + AA, and L+ AA + G groups compared to L group (P<0.05). TUNELL positive cell number in eye retina significantly increased in L group compared to control groups (P<0.05) and decreased in L+ G, L+ AA, and L+AA + G groups compared to L group (P<0.05). Conclusion: Garlic juice and ascorbic acid administration during pregnancy and lactation may protect lead-induced apoptosis in rat offspring''s eye retina. Key Words: Lead, Garlic, Ascorbic acid, Apoptosis, Retina     

Chronic Aerobic Exercise Decreases Lectin-Like Low Density Lipoprotein (LOX-1) Receptor Expression in Heart of Diabetic Rat

Background:

Overexpression of lectin-like low density lipoprotein (LOX-1) receptor plays an important role in hyperglycemia-induced vascular complications such as atherosclerosis. Based on the beneficial effects of exercise on preventing cardiovascular complications of diabetes, we aimed to examine the protective effects of aerobic exercise on expression of LOX-1 receptor and production of free radicals in the heart of diabetic rats.

Methods:

Four groups of rats were used: (n = 5 per group): sedentary normal, trained normal, sedentary diabetes and trained diabetes. Diabetes was induced by a single intraperitoneal injection of streptozotocin (50 mg/kg). The exercise protocol was consisted of swimming 30 min/day, 5 days/week for eight weeks. Plasma glucose was evaluated at initiation, weeks 4 and 8 of experiment. At the end of experiment, rats were sacrificed and the heart was removed for determination of nitrate, malondialdehyde, and LOX-1 gene expression.

Results:

In normal non-diabetic rats, the blood glucose level was <150 mg/dl; however, the induction of diabetes resulted in levels more than >400 mg/dl. Gene expression of LOX-1 was increased in the heart of diabetic rats. Exercise reduced the gene expression of this protein in diabetic states without reducing the blood glucose. Finally, swimming exercise decreased the malondialdehyde and nitrate levels in heart tissue both in control and diabetic rats.

Conclusion:

Swimming exercise reduces heart expression of the LOX-1 receptor in accompany with reduction of free radicals production. Since these parameters are important in generation of diabetic complications, swimming exercise is a good candidate for reducing these complications. Key Words: Hyperglycemia, Diabetic complications, LOX-1 receptor, Exercise, Free radicals