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Background:The worldwide used bisphenol A (BPA) which is incorporated in many plastic industries is considered as an endocrine disruptor. Warnings raised by many agencies against the excessive use of such substances because of its confirmed hazardous effects. Selenium (Se) is known to have antioxidant role in living systems. Aim of the work:The aim of the current study was to evaluate the extent to which BPA can affect the thyroid gland structure and function and if there is any protective role for selenium. Material and Methods: Twenty four adult male rats divided equally into three groups. Group I as a control, group II included rats that received 50 mg/kg/ day bisphenol orally for eight weeks and group III that received bisphenol in the same dose for the same duration concomitantly with selenium in a dose of 0.5 mg/kg. At the end of the experiment, blood samples were taken for hormonal essay and statistical analysis. Thyroid gland tissue samples were processed for histological and immunohistochemical study. Results: BPA-treated rats showed degenerative changes in the form of decreased or absent colloid and fusion of the follicles. Other follicles showed signs of hyperactivity as microfollicles, follicular epithelial cell stratification and many lysosomes. Strong positive inducible nitric oxide synthase immunoreactivity and highly significant increase of serum TSH with decreased T3 and T4 were recorded. BPA+selenium treated group revealed nearly normal appearance of thyroid gland architecture. Conclusion: BPA had deleterious effects on thyroid structure and function. Concomitant administration of selenium preserved to a great extent the thyroid gland architecture.

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Background: Both dermatoglyphics and lip prints/cheiloscopic patterns are genetically determined. Hypertension (HTN) is a major risk factor for cardiovascular disease and causes 17.9 million deaths worldwide each year. Hypertension is also known to have a genetic background as it runs in families.Objectives: This study was conducted to recognize individuals with a genetic predisposition to have hypertension and to determine significant dermatoglyphic parameters and lip print characters applicable to hypertension, also to assess their reliability and validity. Subjects and Methods: 100 female hypertensive patients were taken as the test subjects from the Assiut University Hospital, and an equal number of healthy normotensive volunteers from the general population were utilized as controls. Fingerprint patterns of both groups were recorded using Cummin's method. Then dermatoglyphic analysis was then performed on the prints. Lip impressions were made using red or brown lipstick, A4 size white bond paper, and cellophane tape. The types of grooves were categorized using Suzuki and Tsuchihashi's taxonomy, and the results were statistically examined. Results: Significant dermatoglyphic and cheiloscopic results were detected in the hypertensive group compared to the normotensive control. The data revealed a higher frequency of ulnar loop patterns in both normotensive and hypertensive followed by the whorl and arch fingerprint patterns. A significant decrease in the a-b ridge count and 'atd' angle was declared in the hypertensive group compared to the control. Regarding the cheiloscopic patterns, the obtained data showed significantly higher frequencies of lip-branched patterns and irregular/undifferentiated patterns in the hypertensive group in comparison to the normotensive one. Conclusion: Significant indicators of dermatoglyphic and cheiloscopic features were demonstrated in the hypertensive group compared to the control one. so, they might be employed as a reliable genetic marker for the screening of hypertension.

Gentamicin (GM) is an aminoglycoside that has harmful effects on the male germ cells and sperm quality. N-3 polyunsaturated fatty acids (n-3 PUFA) are natural antioxidants that influence cell signaling and inflammation. Heme-oxygenase-1 (HO-1) and heat shock proteins (HSP) aid in cellular protection against cellular insults. This study aimed to explore the potential alleviating influences of treatment with n-3 PUFA on GM-induced testicular damage. Thirty-two albino male rats were divided into four equal groups. (1) The control group received normal saline, (2) the n-3 PUFA group received 100 mg/kg body weight/day n-3 PUFA daily for 4 weeks, (3) the GM group received 100 mg/kg/day GM intraperitoneally for 10 consecutive days, and (4) the GM + n-3 PUFA group received intraperitoneal GM for ten days followed by treatment with n-3 PUFA for 4 weeks. Significant reductions in sperm motility, viability, serum testosterone, total testicular protein, and germinal epithelium height were observed in the GM-treated group, with upregulation of the oxidative stress markers, HO-1 mRNA, and HSP70, and downregulation of proliferating cell nuclear antigen (PCNA). We also observed cellular disorganization, vacuolation, tubular distortion, and a significantly higher percentage of collagen. Ultra-structurally, most of the spermatogenic cells were electron dense and degenerated with rarefied cytoplasm. Treatment with n-3 PUFA resulted in a significant increase in sperm motility, viability, serum testosterone, and in the germinal epithelium height. Upregulation of HO-1 mRNA, HSP70, and PCNA expression and a significant reduction in the oxidative stress index were also observed. The findings confirm the potential ameliorative role of and imply novel mechanisms by which n-3 PUFA protects against GM-induced testicular injury.

Introduction:It is generally recognised that zinc is an important trace element with crucial functions in cellular metabolism. The liver is responsible for zinc metabolism. Zinc deficiency can cause growth compromised effects in many organs. Objectives: Study of the effects of zinc deficiency on the postnatal development of rat liver using histological and immunohistochemical evaluation. Materials and Methods: Female adult rats, after matting, were allocated randomly into two groups: the control group (24 rats received a single i.p. injection of distilled water on day 9 of gestation) and the experimental group (24 rats i.p. injected 1.10 phenanthroline (zinc chelating agent) in a single dose of 30 mg/kg on day 9 of gestation). Zinc deficiency was confirmed by measuring the serum zinc level in both groups of pregnant females on the 10th day of gestation. Male offspring of treated and control rats were sacrificed at the following postnatal ages: newborn, 15 days, and three months. Samples from the liver were then processed for histological study using light and electron microscopic examination and immunohistochemical evaluation for Bcl2 expression. Results: Light microscopic examination of the treated groups showed a disorganized hepatic architecture with apoptosis of hepatocytes. There was noticeable dilatation and congestion of blood sinusoids and central and portal vessels. Masson's trichrome stain revealed remarkable fibrosis in the treated groups' portal triad. The immunohistochemical study showed weak immunoreactivity for Bcl-2 in zinc deficient groups. The ultrastructural study showed degenerated hepatocytes with cytoplasmic vacuolations. The mitochondria appeared swollen with cristolysis and an electron-dense matrix. Conclusion: Zinc deficiency resulted in deleterious postnatal structural effects on hepatic tissue that affected all age groups and even extended to the adult age.

Methotrexate (MTX) is a chemotherapeutic agent widely used to treat a variety of tumors. Nonetheless, MTX‐induced hippocampal neurotoxicity is a well‐defined dose‐limiting adverse effect that limits clinical utility. Proinflammatory cytokine production and oxidative stress are possible mechanisms for MTX‐induced neurotoxicity. Buspirone (BSP), a partial agonist of the 5‐HT1a receptor (5‐HT1aR), has emerged as an anxiolytic drug. BSP has been shown to possess antioxidant and anti‐inflammatory effects. The current study investigated BSP's potential anti‐inflammatory and antioxidant effects in attenuating MTX‐induced hippocampal toxicity. Rats received either BSP (1.5 mg/kg) orally for 10 days and MTX (20 mg/kg) i.p. on Day 5. BSP administration markedly protected hippocampal neurons from drastic degenerated neuronal changes induced by MTX. BSP significantly attenuated oxidative injury by downregulating Kelch‐like ECH‐associated protein 1 expression while potently elevating hippocampal Nrf2, heme oxygenase‐1, and peroxisome proliferator‐activated receptor expression. BSP dampened inflammation by reducing NO2−, tumor necrosis factor‐alpha, IL‐6, and interleukin 1 beta levels mediated by downregulating NF‐κB and neuronal nitric oxides synthase expression. Moreover, BSP potently counteracted hippocampal pyroptosis by downregulating NLRP3, ASC, and cleaved‐caspase‐1 proteins. Therefore, BSP may represent a promising approach to attenuate neurotoxicity in patients receiving MTX.