Methyl parathion (MP) is an organophosphate pesticide used in agriculture, although quite often illegally used indoors to contain insects. The present study was planned to investigate the effects of MP on rat testis. Adult male Wistar rats (13-14 weeks) were treated with MP as follows. Experiment 1-0, 1.75, 3.5 or 7 mg/kg i.p. for 5 days and sacrificed on Day 14; experiment 2 and 3- 0, 0.5, or 1 mg/kg i.p. for 12 days, and sacrificed on Days 130 and 77, respectively; experiment 4- 0, 0.75, or 1.5 mg/kg i.p. for 25 days, and sacrificed on Day 17; experiment 5- 0 or 3.5 mg/kg po for 25 days, and sacrificed on Day 17, after the last exposure. MP decreased the body weight and the testis weight in experiments 4 and 5 (p5>1>3>2 indicating more effect of prolonged i.p. treatment. Homogenization-resistant spermatid count was decreased in experiments 1, 4 and 5, and MP also decreased the tubular diameter, and epithelial height (p<0.05-0.001). Incidences of stage XIV tubules, number of meiotic figures and elongating spermatids were also decreased, whereas the incidence of tubules showing epithelial sloughing increased (p<0.05-0.001). We conclude that MP is a reproductive toxicant in male rats which causes significant testicular damage in the testis.

Background and Aim: Depression and anxiety are the most prominent neuropsychiatric disease and have been considered as the most burdensome diseases of society. The hippocampus and prefrontal cortex have a prominent role in stress-induced neurological disorders. Chronic unpredictable stress exposed rats are a perfect model in understanding comorbid depression and anxiety disorders. The inflammatory response occurring in the body has been linked to C-reactive protein (CRP) in many diseased conditions. The present research primarily focus on the possible correlation of Cortisol, CRP level and neuronal assay in different regions of hippocampus, dentate gyrus (DG), and prefrontal cortex. Materials and Methods: The control group of rats (n=6) was not exposed to any stress. Whereas, the experimental stress group (n=6) of rats was exposed to various stressors for 15 days. After the experimentation procedures, the blood samples were collected and brain dissection was done. The neurons in the prefrontal cortex, the DG along with various hippocampal regions was counted. Statistical analysis was performed using student's t-test and p<0.05 was expressed as statistically significant. Results: Animals exposed to chronic unpredictable stressors showed a significant (p<0.0001) decrease in the neuronal count in prefrontal cortex and hippocampus. A significant rise in the serum cortisol (p<0.0001) and CRP (p<0.001) was witnessed in the stressed group. Conclusion: Our results demonstrate that chronic unpredictable stress exposure has affected neurogenesis in prefrontal cortex and hippocampal regions. Decreased neurogenesis was well in coordinance with the increase in cortisol and CRP. The chronic unpredictable stress-induced inflammatory response correlated to various brain regions might provoke insights into a variety of new drugs targeting neurogenesis.

Background: In recent years, increased stress in human life has a dual effect on brain and body physiology. Chronic stress takes a toll on physiology as well as on quality of life, ultimately leading to affective disorders. Rodent models are indispensable tools for studying the etiology and progress of depression. C-reactive protein has been proposed as a novel inflammatory marker. Methods: Rats were divided into control and experimental stress groups (n = 6 each). The experimental group consisted of rats that were exposed to a set of chronic unpredictable stressors for 15 days. At the end of the 15th day, the animals were anesthetized, and blood samples were collected through cardiac puncture. Then the blood samples were analyzed for selected biochemical and oxidative stress parameters. Results: Serum glutamic oxaloacetic transaminase (p < 0.0001), serum glutamic pyruvic transaminase (p < 0.001), serum malondialdehyde (p < 0.0001), total antioxidant level (p < 0.0001), and serum cortisol (p < 0.0001) were significantly increased in the stressed group when compared with the control group. C-reactive protein significantly (p < 0.0001) increased in the stressed group when compared with the control group. Conclusion: Our results demonstrate that chronic unpredictable stress ameliorated depression-like behavior, which might have caused the dysregulation of the hypothalamic-pituitary-adrenal axis, causing the imbalance in the biochemical and oxidative parameters increasing the inflammatory markers. The inflammation-induced model of the chronic unpredictable stress model of comorbid depression might provide a variety of new targets for antidepressant therapies.