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In a previous study we demonstrated that repeated maternal separation impaired spatial memory performance in both male and female adolescent rats. The mechanisms of these cognitive alterations are unknown. In the present study, we examined the effects of repeated maternal separation on oxidative stress in the hippocampus, prefrontal cortex and striatum regions of the brain of the adolescent male and female rats. The results showed that repeated maternal separation increased antioxidant enzyme activities and lipid peroxidation in adolescent male rat brains; however, maternal separation did not effects antioxidant enzyme activities and lipid peroxidation in adolescent female rat brains. These results suggest that oxidative stress caused damage in repeated maternal separated adolescent male rat brains, also a strong role of gender in the response of adolescent subjects to maternal separation. [ABSTRACT FROM AUTHOR]

Objectives: It is known that maternal deprivation (MD) may alter cognitive functions such as learning and memory in adult life by effecting normal growth and development. However, the mechanisms of these cognitive alterations are unknown. The aim of this study is to investigate the effects of maternal deprivation on cognition and melatonin production in adolescent male and female rats., Methods: The litters were separated daily from their mothers for 6 hours on postnatal days 2 to 20. The spatial memory performance was evaluated using a Morris water maze between the postnatal 26th and 32nd days. Plasma melatonin levels were determined on postnatal days 42., Results: MD-rats had longer escape latencies at the second, third and fifth days of training days and spend significantly less time in probe trial, compared to control animals., Main Findings: The repeated maternal deprivation caused low blood melatonin levels and there was a significant negative correlation between blood melatonin levels and spatial memory performance in both of male and female adolescent rats., Conclusion: These results suggest an association between melatonin production and neurodevelopment. Further studies are needed to determine the interaction between maternal deprivation and pineal gland maturation/function.

Objectives: L-carnitine is a naturally compound widely distributed in the body. It has an antiradical effect and decreases lipid peroxidation. In acute or chronic streptozotocin (STZ)-induced diabetic rats, the pancreatic content of carnitine was found to be significantly lower than nondiabetic group. We investigated the effects of L-carnitine on the development of STZ-induced diabetes in rats, to determine if L-carnitine can prevent the onset of diabetes or reduce the severity of hyperglycemia and this prevention/reduction is associated with the reduction in oxidative stress., Setting and Design: The rats were divided into 3 groups: Control, STZ-treated (65 mg/kg intraperitoneally) and L-carnitine (500 mg/kg) and STZ-treated., Methods: Oxidative stress was assessed by measuring pancreatic thiobarbituric acid reactive substance (TBARS) formation levels using the method of Rehncrona et al, pancreatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities using a Randox test combination (RANSOD and RANDOX)., Results: L-carnitine did not prevent the onset of diabetes at this dose. Development of diabetes was associated with an increase in pancreatic TBARS (0.028 +/- 0.008 and 0.046 +/- 0.017 nmol/mg Protein, respectively), and GPx activity (0.067 +/- 0.011 and 0.098 +/- 0.016 U/mg Protein, respectively)., Main Findings: L-carnitine prevented this increase induced by diabetes; TBARS (0.039 +/- 0.006 nmol/mg Protein) and GPx activity (0.053 +/- 0.011 U/mg Protein)., Conclusion: These results suggest that L-carnitine exerts anti-oxidative effect in experimental diabetes.