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.

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.

Could Vitamin C Protect Against Mercuric Chloride Induced Lung Toxicity In The Offspring Rat: A Histological And Immunohistochemical Study.

Mercury (Hg) is one of the most toxic heavy metals and widely utilized in various industries. Hg exposure causes serious health impacts through unfavorable pathological and biochemical effects. We aimed to assess the effect of mercuric chloride (HgCl2) prenatal exposure on the lung development and probable prophylactic effect of vitamin C. The 30 pregnant rats were used in this work and divided randomly into 3 equal groups: Group Ӏ given distilled water, Group ӀӀ given HgCl2 at dose of 4 mg/ BW/day and Group ӀӀӀ given HgCl2 and Vitamin C at dose of 200 mg/kg BW/day. The pups of each group at birth were collected, counted and weighted then lung specimens were extracted, weighted, anaesthetized and processed for the light, electron microscopic and immunohistochemical studies. Also, morphometric studies were performed. We found that prenatal HgCl2 exposure caused collapse of alveoli, thick interalveolar septa, degenerated type Ӏ and type Ӏ pneumocytes, extensive extravasation of RBCs, extensive collagen fibers deposition, positive iNOS immunoreaction and significant decrease in the body and lung weights. Vitamin C concomitant administration partially reversed HgCl2 induced lung degeneration. We concluded that prenatal HgCl2 exposure caused lung damage and vitamin C had protective effects against HgCl2 indued pulmonary toxicity.

Cytoprotective effect of garlic alone versus co-administration of garlic and resveratrol in adriamycin-induced lung toxicity in albino rat: light microscopic, ultrastructural and immunohistochemical study.

Adriamycin is a cytotoxic anthracycline antibiotic used to treat a wide variety of cancers. This study was made to detect the possible prophylactic effects of combining garlic and resveratrol in preventing adriamycin-induced pulmonary cytotoxicity. This study was conducted on a total number of 60 adult male albino rats. The rats were divided in an equally random manner into 6 groups: group I rats received nothing, group II received a dose of 50 mg/kg garlic extract orally for 3 weeks, group III received resveratrol in a dose of 20 mg/kg/day orally for 3 weeks, group IV rats were injected with 20 mg/kg adriamycin as a single dose via intraperitoneal route, group V received garlic extract for 3 weeks, then were injected with adriamycin in the same stated doses, and Group VI received garlic extract and resveratrol in same stated dose for 3 weeks, then were injected with adriamycin in the same stated dose. Lung specimens were processed for light microscopic, ultrastructural, and immunohistochemical studies. Adriamycin treatment caused histological alterations, thicker interstitial septa, extensive cellular infiltration, hypertrophied arterial wall, marked inducible Nitric Oxide Synthase immunoreaction, type I pneumocytes with destructed organelles as well as type II pneumocytes having large vacuoles. The combined garlic and resveratrol group demonstrated a considerable improvement in the changes to the histology and ultrastructure of adriamycin-induced lung injury. Combining garlic and resveratrol can prevent adriamycin-induced lung cytotoxicity in albino rats.

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.

Riboflavin attenuates tartrazine toxicity in the cerebellar cortex of adult albino rat.

Tartrazine is a synthetic yellowish dye considered one of the most common food colorants. Extensive usage of tartrazine in humans led to harmful health impacts. To investigate the impact of tartrazine administration on the cerebellum and to assess the potential role of riboflavin co-administration in the adult male albino rat. Four groups of adult albino rats were included in this study. Group I was supplied with distilled water. Group II was supplied tartrazine orally at a dose of 7.5 mg/kg BW dissolved in distilled water. Group III was supplied with tartrazine at the same previously mentioned dose and riboflavin orally at a dose of 25 mg/kg BW dissolved in distilled water. Group IV was supplied with riboflavin at the same previously mentioned dose. The study was conducted for 30 days then rats were sacrificed, weighted and the cerebella extracted and handled for light, ultrastructural and immunohistochemical evaluation. It was found with tartrazine treatment focal areas of Purkinje cell loss leaving empty spaces, a broad spread of neuronal affection to the degree of the disappearance of some of the granular cells, reduced the thickness of the molecular and granular layers, and strong positive GFAP immunoreactions. With riboflavin coadministration restored continuous Purkinje layer with normal appeared Purkinje cells, but some cells were still shrunken and vacuolated as well as the molecular and granular cell layers appeared normal. Tartrazine had deleterious effects on the cerebellar cytoarchitecture, and riboflavin co-administration alleviated these neurotoxic effects.

The teratogenic effect of pregabalin on heart, liver and kidney in rats: a light microscopic, electron microscopic and immunohistochemical study.

BACKGROUND: Pregabalin (PGB) was approved as new anti-epileptic drugs with little information about its teratogenic effect. AIM OF THE WORK: to evaluate the developmental toxicity of PGB. MATERIALS AND METHODS: 60 pregnant albino rats were divided into three groups. PGB (500 mg/kg body weight/day) was given to group II, PGB (1250 mg/kg body weight/day) was given to Group III and no medications were given to group I. The pups were normally delivered. Liver, kidney and heart specimens were prepared for histological, immunohistochemical, and morphometric studies. RESULTS: A dose of 500 mg of PGB had minimal toxic effects in the form of mild collagen deposition and moderate positive caspase-3 immunoexpression. PGB dose of 1250 mg/kg induced gross toxic effects in form of degenerated cardiac myofibres, ruptured blood vessels, vacuolations in the renal cortex, fibrosis and strong positive caspase-3 immunoexpression. CONCLUSION: PGB at dose of 500 mg/kg revealed minimal toxic changes. PGB cause embryotoxicity in a dose-dependent manner, as the higher dose induced more degenerative changes.

Glucagon-like peptide-1 analog improves neuronal and behavioral impairment and promotes neuroprotection in a rat model of aluminum-induced dementia.

BACKGROUND: Alzheimer's disease (AD) is a worldwide severe medical and social burden. Liraglutide (LIR) has neuroprotective effects in preclinical animal models. AIM: To explore the probable neuroprotective impact of Glucagon-like peptide-1 (GLP-1) on rats' behavior and to elucidate its underlying mechanisms. METHODS: A total of 24 male albino rats were assigned to control, LIR (300 µg/kg subcutaneously (s.c.)), AD only (100 mg/kg aluminum chloride (AlCl3 ) orally) and LIR + AD treated groups. Eight radial arm maze was performed. Serum blood glucose, proinflammatory cytokines, oxidative stress markers were measured and hippocampal tissue homogenate neurotransmitters were evaluated. Histopathological and immunofluorescent examinations were performed. RESULTS: LIR prevents the impairment of learning and improves both working memory and reference memory through significant reduction of serum tumor necrosis factor (TNF-α), interleukin 6 (IL-6) and interferon-γ (INF-γ) and malondialdehyde (MDA) and through the increase of superoxide dismutase (SOD), dopamine, adrenaline, and noradrenaline. LIR also improves hippocampal histological features of ALCL3 administrated rats and decreases the percentage of neuronal loss. CONCLUSION: LIR normalizes ALCL3 -induced dementia. It improves cognitive dysfunction and ameliorates cerebral damage.