No abstract

Increased infertility in humans is attributed to the increased use of environmental chemicals in the last several decades. Various studies have identified pesticides as one of the causes of reproductive toxicity. In a previous study, infertility was observed in male mice due to testicular atrophy and decreased sperm count when a sublethal dose of endosulfan (3 mg/kg) with a serum concentration of 23 μg/L was used. However, the serum concentration of endosulfan was much higher (up to 500 μg/L) in people living in endosulfan-exposed areas compared to the one used in the investigation. To mimic the situation in an experimental setup, mice were exposed to 5 mg/kg body weight of endosulfan, and reproductive toxicity and long-term impact on the general biology of animals were examined. HPLC analysis revealed a serum concentration of ∼50 μg/L of endosulfan after 24 h endosulfan exposure affected the normal physiology of mice. Histopathological studies suggest a persistent, severe effect on reproductive organs where vacuole degeneration of basal germinal epithelial cells and degradation of the interstitial matrix were observed in testes. Ovaries showed a reduction in the number of mature Graafian follicles. At the same time, mild vacuolation in liver hepatocytes and changes in the architecture of the lungs were observed. Endosulfan exposure induced DNA damage and mutations in germ cells at the molecular level. Interestingly, even after 8 months of endosulfan exposure, we observed increased DNA breaks in reproductive tissues. An increased DNA Ligase III expression was also observed, consistent with reported elevated levels of MMEJ-mediated repair. Further, we observed the generation of tumors in a few of the treated mice with time. Thus, the study not only explores the changes in the general biology of the mice upon exposure to endosulfan but also describes the molecular mechanism of its long-term effects.

<p class="abstract"><strong>Background:</strong> The present study was conducted to elucidate the genes and its associated pathways delineating the growth-promoting potential of polyherbal formulation (PHF), Kolin Plus^TM using microarray in Cobb 430 broiler chickens.</p><p class="abstract"><strong>Methods:</strong> Microarray was performed for<strong> </strong>four groups, namely, normal diet (ND) as G1, choline chloride deficient (CCD) diet as G2, choline chloride (CCL, 400 g/ton) as G3 and PHF (400 g/ton) as G4. Breast muscle samples were collected, and the growth-related gene expression profile was measured using the Agilent microarray platform.  </p><p class="abstract"><strong>Results:</strong> Totally 2900 differentially expressed genes (DEGs) in muscle tissue sample was revealed using hierarchical clustering based on the similarity of their expression profiles, which further allows the user to pick out groups of similar genes. Among them, 1000, 364 and 481 genes were significantly upregulated and 244, 485 and 326 genes were significantly downregulated between ND and CCD, CCL and CCD, PHF and CCD respectively. Furthermore, some of the focused genes (CSRP3, SOX10, BCO1, CALB1, LMOD2, KLF15, CTHRC1, PHGDH, UTS2R, and ANKRD2) were significantly (p&lt;0.05) modulated by PHF (400 g/ton) supplementation in birds fed with CCD diet. These genes play an essential role in protein translation, energy metabolism, and muscle growth promotion.</p><strong>Conclusions:</strong>It may be concluded that supplementation of PHF at 400 g/ton of feed could positively influence the certain focused genes associated with muscle growth promotion, which favours the productive phenotypic response in broiler chickens fed with CCD diet. <p> </p>