Ameliorative effects of gallic acid on tebuconazole-induced adverse effects in the cerebellum of adult albino rats: histopathological and immunohistochemical evidence.

Tebuconazole (TEB) is a common triazole sterol demethylation inhibitor fungicide utilized to manage a variety of diseases in crops like cereals, fruits, and vegetables. The aim of this work was to assess the effects of TEB on the structure of the cerebellum in adult albino rats and possible protective impact of co-administration of Gallic acid (GA). Four groups of forty adult male albino rats were randomly selected, and the rats in group I received corn oil through daily gavage for 4 weeks. Group II received GA dissolved in the normal saline at a dose of 100 mg/kg through daily gavage for 4 weeks, group III administered with TEB dissolved in corn oil at its acceptable daily intake dose (0.02 mg/kg body weight) through daily gavage for 4 weeks, group IV rats received both TEB and GA. For light microscopic, ultrastructural, and immunohistochemical investigations, cerebellar specimens were prepared. TEB exposure led to neuronal damage in the form of degenerated Purkinje cells with vacuolated cytoplasm, areas of lost Purkinje cells, the basket cells appeared vacuolated with degenerated neuropil, the granule cells clumped with congested areas between them, dilated cerebellar islands, weak positive bcl2 immunoreactions in the Purkinje cells, and numerous GFAP-positive astrocytes. GA mitigated TEB-mediated histological changes in the cerebellar cortex. We concluded that TEB caused Purkinje neurons in the rat cerebellar cortex to degenerate and undergo apoptosis. GA had a neuroprotective benefit against TEB toxicity in the rat cerebellar cortex.

Resveratrol ameliorates atrazine-induced caspase-dependent apoptosis and fibrosis in the testis of adult albino rats.

Pesticides like atrazine which are frequently present in everyday surroundings, have adverse impacts on human health and may contribute to male infertility. The work aimed to analyze the histological and biochemical effects of atrazine on the testis in adult albino rats and whether co-administration with resveratrol could reverse the effect of atrazine. Forty adult male albino rats in good health participated in this study. They were categorized at random into four groups: the Group Ӏ received water through a gastric tube for two months every day, the Group ӀӀ received resveratrol (20 mg/kg body weight (b.w.)) through a gastric tube for two months every day, the Group ӀӀӀ received atrazine (50 mg/kg bw) through a gastric tube for two months every day, the Group ӀV received concomitant doses of atrazine and resveratrol for two months every day. The testes of the animals were then carefully removed and prepared for biochemical, immunohistochemical, light, and electron microscopic studies. Atrazine exposure led to a significant decrease in serum testosterone hormone level, upregulation of caspase 3 and iNOS mRNA levels, destructed seminiferous tubules with few sperms in their lumens, many collagen fibres accumulation in the tunica albuginea and the interstitium, abnormal morphology of some sperms as well as many vacuolations, and damaged mitochondria in the cytoplasm of many germ cells. Concomitant administration of resveratrol can improve these adverse effects. It was concluded that atrazine exposure is toxic to the testis and impairs male fertility in adult rat and coadministration of resveratrol guards against this toxicity.

The possible protective role of selenium on the visual cortex of adult albino rat on exposure to potassium dichromate.

The visual cortex is very important in mammals for processing of visual information. Exposure to heavy metals such as potassium dichromate poses serious health threat to human beings. The aim of this work is to study the effect of potassium dichromate on the visual cortex of adult albino rat and also to identify the possibility of selenium as protective agent against toxicity of potassium dichromate. A total number of 40 adult albino rats weighting (200-250) gm were used. They divided into four groups: control group, potassium dichromate received group, potassium dichromate and selenium received group and selenium received group. The rats received treatment for 6 weeks. After 6 weeks, they were sacrificed. The present study showed that potassium dichromate causes degeneration of granular neurons in layer IV and pyramidal neurons in layer V. Morphometric results revealed statistically significant decrease in the number of granule and pyramidal cells in potassium dichromate received group as compared with control group. Most of degenerative changes are improved by selenium.

الدور الوقائي المحتمل للسيلينيوم على القشرة المخية البصرية للفأر الابيض البالغ عند التعرضللدايكرومات البوتاسيومسالي سيد أنور-هالة محمد حسانينقسم التشريح الادمي وعلم الاجنة -كلية الطب البشرى- جامعة اسيوطالقشرة البصرية مهمة جدا في الثدييات لمعالجة المعلومات المرئية. يشكل التعرض للمعادنالثقيلة مثل ثنائي كرومات البوتاسيوم تهديداً صحياً خطيراً للإنسان. الهدف من هذا العمل هودراسة تأثير ثنائي كرومات البوتاسيوم على القشرة البصرية لجرذ ألبينو البالغ وكذلك التعرفعلى إمكانية استخدام السيلينيوم كعامل وقائي ضد سمية ثنائي كرومات البوتاسيوم. تم استخدامجرذ من الجرذان البالغة وزنها (200-250) جرام. تم تقسيمهم إلى 4 مجموعات: المجموعة40الضابطة ، المجموعة المستلمة ثنائي كرومات البوتاسيوم ، المجموعة المستلمة ثاني كروماتالبوتاسيوم والسيلينيوم المجموعة المستلمة سيلينيوم تلقتالفئران العلاج لمدة 6أسابيع. بعد ستة أسابيع تم التضحية بهم. أظهرت الدراسة الحالية أن ثنائي كرومات البوتاسيوميسبب تنكس الخلايا العصبية الحبيبية في الطبقة الرابعة والخلايا العصبية الهرمية في الطبقةالخامسة. أظهرت نتائج القياس المورفومتري انخفاضًا ذا دلالة إحصائية في عدد الخلايا الحبيبيةوالهرمية في المجموعة التي تم تلقيها من ثنائي كرومات البوتاسيوم مقارنة بمجموعة التحكم. يتمتحسين معظم التغييرات التنكسية بواسطة السيلينيوم.[Figure: see text].

Could vitamin D protect against high fat diet induced damage in the arcuate nucleus in the rat: histological, immunohistochemical and ultrastructural study.

Obesity is a serious health issue. As regard, the central nervous system, obesity induces neuronal damage. Vitamin D has well-known anti-inflammatory and neuroprotective effects. To detect if vitamin D protects against damage in the arcuate nucleus induced by a high fat-high fructose diet. Forty adult rats were used, and four groups were formed. Group I (negative control) kept on a standard chow diet for six weeks, Group II (positive control) received vitamin D orally once every other day for six weeks, Group III (high fat-high fructose treated group) was given high fat-high fructose diets for six weeks and Group IV (high fat-high fructose and vitamin D treated group) were given high fat-high fructose diets concomitantly with vitamin D for six weeks. High fat-high fructose diet markedly caused histological changes in arcuate neurons as nuclei appeared darkly stained and shrunken with condensed chromatin, and the nucleolus became less prominent. The cytoplasm appeared rarefied with loss of most of the organelles. An increase in neuroglial cells was noticed. The synaptic area showed sparse degenerated mitochondria and a disrupted presynaptic membrane. A high-fat diet has a damaging effect on arcuate neurons and vitamin D alleviates these effects.