Unilateral orchidectomy (UO) is required when further breeding potential is important. It is sometimes necessary to remove a single testis in a matured stallion for therapeutic reasons. In this study, twelve donkeys were used to evaluate three techniques of unilateral castration, histological and morphological changes on the remaining testis. Results of the study showed that each of the surgical techniques used had its advantages and disadvantages in comparison with the other two techniques. Therefore the selection among the three techniques depends on the surgeon preferences and the environment in which the unilateral orchidectomy is performed. The volume of the remaining testis recorded at the end of the study was significantly greater than that estimated at the start of the study (p 0.05). The percentage of sperm motility obtained from the remaining testis was significantly decreased (p 0.05). Histological examination of the testis in open surgery (group I) (where the scrotum was left opened) revealed severe hemorrhages, edema and fibrosis. The test is showed degenerative changes in the seminiferous tubules and interstitial orchitis. Histological examination of the testes removed using a closed technique, (in groups II and III) where the scrotum wound was sutured, revealed hyperplasia of spermatogenic series and Leydig cells. In conclusion, unilateral orchidectomy had compensatory effects on the weight and volume of remaining testis. Adverse effects on sperm motility and viability can affect the fertility of the animal.

Even though rotenone has been used extensively in recent years to produce a model of Parkinson disease in rats, its systemic effects either on neurons apart from dopaminergic structures or non-neuronal tissues have not been elucidated well. In our present study, 30 adult Sprague-Dawley rats were divided into three even groups. A short-term rotenone-treated group received 10mg/kg b.w. rotenone daily for 7 days. The long-term rotenone-treated group received 3mg/kg b.w. rotenone daily for 30 days. The control group received vehicle only and were kept 5 rats each in parallel to both short- and long-term rotenone treated groups. It was found that short-term rotenone treatment produced marked vascular damages associated with ischemic neuronal degeneration particularly in the thalamus, cerebellum and nucleus dentatus. In long-term rotenone-treated group, vascular changes were less severe and neuronal degeneration was associated with mild microglial proliferation and astrocytosis. Non-neuronal pathology as the result of short-term rotenone exposure consisted of degeneration and necrosis of seminiferous tubular epithelia with formation of spermatide multinucleate giant cells. On the other hand, long-term rotenone treatment did not affect testicles and only caused sinusoidal dilatation in the liver, myocardial degeneration in the heart and interstitial hemorrhages in the kidneys and lungs. In conclusions, damage to blood vasculature by rotenone appeared mediating neuronal and non-neuronal pathology in Sprague-Dawley rats. This effect might provide new insights for ethiopathogenesis of neurodegenerative diseases and contributes to the understanding of hemorrhagic stroke.Even though rotenone has been used extensively in recent years to produce a model of Parkinson disease in rats, its systemic effects either on neurons apart from dopaminergic structures or non-neuronal tissues have not been elucidated well. In our present study, 30 adult Sprague-Dawley rats were divided into three even groups. A short-term rotenone-treated group received 10mg/kg b.w. rotenone daily for 7 days. The long-term rotenone-treated group received 3mg/kg b.w. rotenone daily for 30 days. The control group received vehicle only and were kept 5 rats each in parallel to both short- and long-term rotenone treated groups. It was found that short-term rotenone treatment produced marked vascular damages associated with ischemic neuronal degeneration particularly in the thalamus, cerebellum and nucleus dentatus. In long-term rotenone-treated group, vascular changes were less severe and neuronal degeneration was associated with mild microglial proliferation and astrocytosis. Non-neuronal pathology as the result of short-term rotenone exposure consisted of degeneration and necrosis of seminiferous tubular epithelia with formation of spermatide multinucleate giant cells. On the other hand, long-term rotenone treatment did not affect testicles and only caused sinusoidal dilatation in the liver, myocardial degeneration in the heart and interstitial hemorrhages in the kidneys and lungs. In conclusions, damage to blood vasculature by rotenone appeared mediating neuronal and non-neuronal pathology in Sprague-Dawley rats. This effect might provide new insights for ethiopathogenesis of neurodegenerative diseases and contributes to the understanding of hemorrhagic stroke.

Even though rotenone has been used extensively in recent years to produce a model of Parkinson disease in rats, its systemic effects either on neurons apart from dopaminergic structures or non-neuronal tissues have not been elucidated well. In our present study, 30 adult Sprague-Dawley rats were divided into three even groups. A short-term rotenone-treated group received 10mg/kg b.w. rotenone daily for 7 days. The long-term rotenone-treated group received 3mg/kg b.w. rotenone daily for 30 days. The control group received vehicle only and were kept 5 rats each in parallel to both short- and long-term rotenone treated groups. It was found that short-term rotenone treatment produced marked vascular damages associated with ischemic neuronal degeneration particularly in the thalamus, cerebellum and nucleus dentatus. In long-term rotenone-treated group, vascular changes were less severe and neuronal degeneration was associated with mild microglial proliferation and astrocytosis. Non-neuronal pathology as the result of short-term rotenone exposure consisted of degeneration and necrosis of seminiferous tubular epithelia with formation of spermatide multinucleate giant cells. On the other hand, long-term rotenone treatment did not affect testicles and only caused sinusoidal dilatation in the liver, myocardial degeneration in the heart and interstitial hemorrhages in the kidneys and lungs. In conclusions, damage to blood vasculature by rotenone appeared mediating neuronal and non-neuronal pathology in Sprague-Dawley rats. This effect might provide new insights for ethiopathogenesis of neurodegenerative diseases and contributes to the understanding of hemorrhagic stroke.Even though rotenone has been used extensively in recent years to produce a model of Parkinson disease in rats, its systemic effects either on neurons apart from dopaminergic structures or non-neuronal tissues have not been elucidated well. In our present study, 30 adult Sprague-Dawley rats were divided into three even groups. A short-term rotenone-treated group received 10mg/kg b.w. rotenone daily for 7 days. The long-term rotenone-treated group received 3mg/kg b.w. rotenone daily for 30 days. The control group received vehicle only and were kept 5 rats each in parallel to both short- and long-term rotenone treated groups. It was found that short-term rotenone treatment produced marked vascular damages associated with ischemic neuronal degeneration particularly in the thalamus, cerebellum and nucleus dentatus. In long-term rotenone-treated group, vascular changes were less severe and neuronal degeneration was associated with mild microglial proliferation and astrocytosis. Non-neuronal pathology as the result of short-term rotenone exposure consisted of degeneration and necrosis of seminiferous tubular epithelia with formation of spermatide multinucleate giant cells. On the other hand, long-term rotenone treatment did not affect testicles and only caused sinusoidal dilatation in the liver, myocardial degeneration in the heart and interstitial hemorrhages in the kidneys and lungs. In conclusions, damage to blood vasculature by rotenone appeared mediating neuronal and non-neuronal pathology in Sprague-Dawley rats. This effect might provide new insights for ethiopathogenesis of neurodegenerative diseases and contributes to the understanding of hemorrhagic stroke.

Curcumin, the yellow spice derived from the roots (rhizomes) of the plant Curcuma longa, has been reported to have a chemoprotective effect against several neoplasms. The protective effect of curcumin during N-nitrosodiethylamine- and carbon tetrachloride-induced hepatocarcinogenesis in Sprague–Dawley rats and its effect on the expression of IkappaB-alpha mRNA were evaluated. Sixty male rats were randomly assigned into four experimental groups. Group A animals received a single i.p. injection of N-nitrosodiethylamine (200 mg/kg b.w.). After 1 week, the animals received weekly s.c. injections of carbon tetrachloride (3 ml/kg b.w./week) for 6 weeks. Group B was given diet containing 0.2 % curcumin 2 weeks before the injection of N-nitrosodiethylamine and continued throughout the experimental period (20 weeks). Group C was given only a diet containing 0.2 % curcumin for the whole period of the experiment. Group D animals served as control. The level of IkappaB-alpha (IкB-α) mRNA was determined by semiquantitative PCR. Administration of diet containing 0.2 % curcumin, 2 weeks before the injection of N-nitrosodiethylamine and throughout the period of experiment, decreased percentage of preneoplastic foci in hepatic parenchyma and inhibited the development of hepatocellular carcinoma, cholangiofibrosis, and cystic cholangioma in rat liver. Moreover, curcumin administration decreased the number and size of the preneoplastic foci induced by N-nitrosodiethylamine and carbon tetrachloride in the liver. The densitometric analysis of the IкB-α mRNA bands revealed that curcumin administration blocked the decrease of IкB-α mRNA induced by N-nitrosodiethylamine and carbon tetrachloride. These results concluded that curcumin inhibited hepatocarcinogenesis induced by N-nitrosodiethylamine and carbon tetrachloride through blocking IкB-α degradation.

Curcumin, the yellow spice derived from the roots (rhizomes) of the plant Curcuma longa, has been reported to have a chemoprotective effect against several neoplasms. The protective effect of curcumin during N-nitrosodiethylamine- and carbon tetrachloride-induced hepatocarcinogenesis in Sprague–Dawley rats and its effect on the expression of IkappaB-alpha mRNA were evaluated. Sixty male rats were randomly assigned into four experimental groups. Group A animals received a single i.p. injection of N-nitrosodiethylamine (200 mg/kg b.w.). After 1 week, the animals received weekly s.c. injections of carbon tetrachloride (3 ml/kg b.w./week) for 6 weeks. Group B was given diet containing 0.2 % curcumin 2 weeks before the injection of N-nitrosodiethylamine and continued throughout the experimental period (20 weeks). Group C was given only a diet containing 0.2 % curcumin for the whole period of the experiment. Group D animals served as control. The level of IkappaB-alpha (IкB-α) mRNA was determined by semiquantitative PCR. Administration of diet containing 0.2 % curcumin, 2 weeks before the injection of N-nitrosodiethylamine and throughout the period of experiment, decreased percentage of preneoplastic foci in hepatic parenchyma and inhibited the development of hepatocellular carcinoma, cholangiofibrosis, and cystic cholangioma in rat liver. Moreover, curcumin administration decreased the number and size of the preneoplastic foci induced by N-nitrosodiethylamine and carbon tetrachloride in the liver. The densitometric analysis of the IкB-α mRNA bands revealed that curcumin administration blocked the decrease of IкB-α mRNA induced by N-nitrosodiethylamine and carbon tetrachloride. These results concluded that curcumin inhibited hepatocarcinogenesis induced by N-nitrosodiethylamine and carbon tetrachloride through blocking IкB-α degradation.

Aims: Asthma is an inflammatory lung disease characterized by bronchoconstriction and hyper responsiveness. Immuno stimulatory effects of melatonin have been reported. In this study, we investigated the impact of melatonin administration on allergic airway inflammation in a rat model. Methods: Forty five adult Wistar albino rats were equally divided into three groups: group I served as control; group II: rats sensitized to ovalbumin and challenged intranasally with ovalbumin to induce an allergic inflammatory response and group III, rats were sensitized and treated with intraperitoneally melatonin. The serum levels of IgE, IgG1 and ova-specific IgG were measured by ELISA. In the bronchoalveolar lavage fluid (BALF), the levels of IL-4, IL-5, IL-13, 1L-10 were measured. IL-10 expression was measured by real time polymerase chain reaction. Histopathological examination of the lung tissues using H&E stain were done. Results: Melatonin administration inhibited allergen-induced lung eosinophilic infiltration and improved the pathological lesions of the lungs. It significantly decreased total serum IgE, IgG1 and OVA-specific IgG1 along with BALF levels of IL-4, IL-5, IL-13. Melatonin increased BALF levels of IL-10 and its mRNA expression. Conclusion: Melatonin administration exhibited a significant reduction in all the markers of allergic inflammation. The data suggests that inhibition of T-cell response and up regulation of IL-10 may be responsible for immunomodulatory effect of melatonin in the rat model of allergic airway inflammation.

Aims: Asthma is an inflammatory lung disease characterized by bronchoconstriction and hyper responsiveness. Immuno stimulatory effects of melatonin have been reported. In this study, we investigated the impact of melatonin administration on allergic airway inflammation in a rat model. Methods: Forty five adult Wistar albino rats were equally divided into three groups: group I served as control; group II: rats sensitized to ovalbumin and challenged intranasally with ovalbumin to induce an allergic inflammatory response and group III, rats were sensitized and treated with intraperitoneally melatonin. The serum levels of IgE, IgG1 and ova-specific IgG were measured by ELISA. In the bronchoalveolar lavage fluid (BALF), the levels of IL-4, IL-5, IL-13, 1L-10 were measured. IL-10 expression was measured by real time polymerase chain reaction. Histopathological examination of the lung tissues using H&E stain were done. Results: Melatonin administration inhibited allergen-induced lung eosinophilic infiltration and improved the pathological lesions of the lungs. It significantly decreased total serum IgE, IgG1 and OVA-specific IgG1 along with BALF levels of IL-4, IL-5, IL-13. Melatonin increased BALF levels of IL-10 and its mRNA expression. Conclusion: Melatonin administration exhibited a significant reduction in all the markers of allergic inflammation. The data suggests that inhibition of T-cell response and up regulation of IL-10 may be responsible for immunomodulatory effect of melatonin in the rat model of allergic airway inflammation.

This study was conducted to investigate the possible protective role of thymoquinone (TQ) and l-cysteine on the reproductive toxicity of male rats induced by cadmium chloride (CdCl2). Forty rats were divided into four even groups. The first group served as untreated control. The second, third and fourth groups received CdCl2, CdCl2 and TQ, and CdCl2 and l-cysteine, respectively for 56 days. Cd exposure caused spermatological damage (decrease sperm count and motility and increased the rates of sperm abnormalities), decrease serum testosterone level and increased oxidative stress. Histological alterations were also observed in the form of vascular and cellular changes in CdCl2 treated rats. The vascular changes were congestion of the blood vessels with interstitial edema in the testes, epididymis, seminal vesicle and prostate. The cellular changes were in the form of degenerative changes with presence of multinucleated giant cells in the lumen of seminiferous tubules, vacuolation and sloughing of the lining epithelium of the epididymis, seminal vesiculitis and prostatitis. Co-administration of TQ and l-cysteine with CdCl2 increased glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and testosterone and reduced lipid peroxidation (LPO) activity. In conclusion, our results showed that TQ and l-cysteine can ameliorate the deleterious effects of CdCl2 probably by activating testicular endocrine and antioxidant systems.

This study was conducted to investigate the possible protective role of thymoquinone (TQ) and l-cysteine on the reproductive toxicity of male rats induced by cadmium chloride (CdCl2). Forty rats were divided into four even groups. The first group served as untreated control. The second, third and fourth groups received CdCl2, CdCl2 and TQ, and CdCl2 and l-cysteine, respectively for 56 days. Cd exposure caused spermatological damage (decrease sperm count and motility and increased the rates of sperm abnormalities), decrease serum testosterone level and increased oxidative stress. Histological alterations were also observed in the form of vascular and cellular changes in CdCl2 treated rats. The vascular changes were congestion of the blood vessels with interstitial edema in the testes, epididymis, seminal vesicle and prostate. The cellular changes were in the form of degenerative changes with presence of multinucleated giant cells in the lumen of seminiferous tubules, vacuolation and sloughing of the lining epithelium of the epididymis, seminal vesiculitis and prostatitis. Co-administration of TQ and l-cysteine with CdCl2 increased glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and testosterone and reduced lipid peroxidation (LPO) activity. In conclusion, our results showed that TQ and l-cysteine can ameliorate the deleterious effects of CdCl2 probably by activating testicular endocrine and antioxidant systems.

The present study aims to investigate the protective effects of thymoquinone, the major active ingredient of Nigella sativa seeds, against lead-induced brain damage in Sprague-Dawley rats. In which, 40 rats were divided into four groups (10 rats each). The first group served as control. The second, third and fourth groups received lead acetate, lead acetate and thymoquinone, and thymoquinone only, respectively, for one month. Lead acetate was given in drinking water at a concentration of 0.5 g/l (500 ppm). Thymoquinone was given daily at a dose of 20 mg/kg b.w. in corn oil by gastric tube. Control and thymoquinone-treated rats showed normal brain histology. Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degeneration of hippocampal and cerebellar neurons, and axonal demyelination. On the other hand, co-administration of thymoquinone with lead acetate markedly decreased the incidence of lead acetate-induced pathological lesions. Thus the current study shed some light on the beneficial effects of thymoquinone against neurotoxic effects of lead in rats.The present study aims to investigate the protective effects of thymoquinone, the major active ingredient of Nigella sativa seeds, against lead-induced brain damage in Sprague-Dawley rats. In which, 40 rats were divided into four groups (10 rats each). The first group served as control. The second, third and fourth groups received lead acetate, lead acetate and thymoquinone, and thymoquinone only, respectively, for one month. Lead acetate was given in drinking water at a concentration of 0.5 g/l (500 ppm). Thymoquinone was given daily at a dose of 20 mg/kg b.w. in corn oil by gastric tube. Control and thymoquinone-treated rats showed normal brain histology. Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degeneration of hippocampal and cerebellar neurons, and axonal demyelination. On the other hand, co-administration of thymoquinone with lead acetate markedly decreased the incidence of lead acetate-induced pathological lesions. Thus the current study shed some light on the beneficial effects of thymoquinone against neurotoxic effects of lead in rats.