Background: Fluoxetine, a selective serotonin reuptake inhibitor, is the most commonly prescribed antidepressant drug for pregnant women. Studies regarding the teratogenic effect of fluoxetine on human and animal models are mainly concerned with structural malformation (congenital anomalies). Aim: Hence, the present study was planned to evaluate the postnatal behavioral effects of fluoxetine on albino rats. Methods: Three groups of female rats received either distilled water or doses of fluoxetine 8 and 12 mg/kg orally from the 6th to the 20th day of pregnancy. Weaning of the pups was done on the 21st day followed by a battery of behavioral tests to assess for any behavioral effect. The tests included negative geotaxis, open field exploration, rota-rod test, elevated plus maze and passive avoidance test. Results: In the present study there was no change in the gestational length of pregnancy, no premature birth or miscarriage during pregnancy. A high dose of in utero fluoxetine resulted in a decrease in birth weight of the offspring and also reduced weight gain during the preweaning period. No major congenital abnormalities were observed in the offspring exposed to fluoxetine. Prenatal fluoxetine exposure at high dose caused an initial transient delay in motor development and this poor motor activity was transient and not permanent. However, prenatal exposure to fluoxetine at a higher dose showed a favorable effect on learning and memory in water maze and passive avoidance tests. Conclusions: From the present study, it may be concluded that prenatal fluoxetine causes a transient delay in motor development but does not adversely affect the postnatal behavioral consequences.

Background: Down syndrome (DS) is the most common chromosomal anomaly associated with mental retardation. This is due to the occurrence of free trisomy 21 (92-95%), mosaic trisomy 21 (2-4%) and translocation (3-4%). Advanced maternal age is a well documented risk factor for maternal meiotic nondisjunction. In India three children with DS are born every hour and more DS children are given birth to by young age mothers than by advanced age mothers. Therefore, detailed analysis of the families with DS is needed to find out other possible causative factors for nondisjunction.

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Introduction. The pathogenesis of type 2 diabetes mellitus (T2DM) is strongly linked to oxidative stress mainly caused by chronic hyperglycaemia. The present study investigates the association between hyperglycaemia with oxidative stress markers, antioxidants and lipid profile. Materials and methods. The case-control study involved two groups, T2DM patients (n = 83) and age and sex matched controls (n = 81). Serum levels of various molecular markers malondialdehyde (MDA), reactive oxygen species (ROS) and nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), vitamin C, total antioxidant capacity (TAC) and lipid parameters total cholesterol, triglycerides, low density lipoprotein (LDL) and high density lipoprotein (HDL) were measured using spectrophotometric assays. Results were analysed to compare and correlate glycaemic levels with these molecular markers. Results. T2DM patients had a higher body mass index (BMI) and body fat percentage. 2 hour blood glucose, glycated haemoglobin A 1c % (HbA 1c), total cholesterol, triglycerides and LDL were higher in diabetics, HDL was found to be lower in diabetics than in controls. Mean levels of enzymatic and non-enzymatic antioxidants SOD, CAT, GSH, vitamin C and TAC were significantly lower while oxidative stress markers NO, ROS and MDA were higher in T2DM patients. NO showed a positive correlation (r = 0.3993, p < 0.0001) whereas TAC showed a negative correlation with glycaemia (r =-0.4796, p < 0.0001). Conclusions. Poor glycaemic control in T2DM causes elevated ROS and NO levels with increased lipid peroxidation and lowered antioxidant capacity. MDA and NO being the major risk factors could be used as a parameter along with antioxidants to assess oxidative stress in T2DM patients.

Recurrent pregnancy loss usually results from disorders that cause intrauterine fetal damage, such as maternal or paternal chromosomal abnormalities. About 15 to 20 percent of all recognized pregnancies end in a first-trimester spontaneous abortion. Parents who are carriers of structural abnormalities have a higher risk of miscarriage because of the aberrations in genetic information may not segregate properly into the reproductive cells. This may be due to translocations, inversions, deletions, and duplications causing pregnancy loss. It is believed that between 3 and 5 percent of recurrent miscarriages are due to genetic factors, about 7 percent are caused by chromosome defects, 15 percent to hormonal defects, and 10 to 15 percent to anatomical defects. The most common cause of early pregnancy losses are chromosomal abnormalities that occur by chance, except in the case of parental chromosomal rearrangements and are not under any controllable influences. This review focuses on the genetic and molecular abnormalities that may contribute to this clinical problem and delineates strategies for genetic evaluation and clinical management in subsequent pregnancies