Morphological changes induced in the brain of rats exposed prenatally to iron and the possible protective role of folic acid

Iron supplementation is recommended during pregnancy to meet the demands of both the mother and rapidly growing fetus. However, newborns and particularly preterm infants are highly susceptible to free radical oxidative damage resulting from iron. Folic acid supplementation is needed during pregnancy and it has been shown to reduce the tissue damage resulting from iron induced oxidative stress. Thirty pregnant female albino rats were used in this experiment and divided into three groups [A, B, C]. Group [A]: Was kept as control. Group [B]: Treated with iron gluconate orally in a dose of 50 mg/kg for eleven days [from day 6-16] of gestation. Group [C]: Treated with the same dose of iron glunonate concomitantly with folic acid in a dose of 5mg/kg for the same previous duration. Samples from the brain striatum of newborns were taken and processed for light and electron microscopic investigation. The light microscopic examination of striatal area of group [B] showed necrotic changes appeared in some neurons in the form of shrinkage and condensation in their nuclei, others appeared degenerated with irregular nuclear outline and multiple vacuoles in their cytoplasm. Aggregated glial cells were observed around the blood capillary and mitotic division could be detected in some of them. Enhanced level of glial fibrillary acidic protein [GFAP] was observed in comparison to control group. Multiple iron deposits in the cytoplasm of neurons and glial cells were observed in group [B] animals. Marked improvement was observed in both neurons and glial cells of group [C]. Electron microscopy revealed apoptotic changes affecting mainly glial cells and some neurons in group [B] associated with swelling of Golgi cisternae and vacuolated mitochondria. Marked improvement was observed in both neurons and glial cells of group [C]. These results indicate that folic acid appears to reduce the iron induced neuronal damage in the brain of newly born rats exposed prenatally to iron

Toxic effect of cisplatin on cerebellar cortex and spinal cord of adult male albino rat and the possible role of vitamin E: light and electron microscopic study

The nervous system is frequently the site of symptomatic toxicity of antineoplastic agents, cisplatin is a widely used potent chemotherapeutic agent that is highly neurotoxic. It has been proven that it is able to generate reactive oxygen species and inhibit the activity of antioxidant enzymes. This study was carried out to demonstrate the neurotoxic effects of cisplatin on the structure of adult rat cerebellum and spinal cord, and the role of vitamin E which has been shown to ameliorate hephro, oto and neurotoxicities induced by cisplatin. Thirty adult male albino rats weighing 200-250 gm were divided into three groups: Group one: kept as a control. Group two: animals treated with cisplatin at a dose of 4mg/kg twice weekly by intraperitoneal injection, for one month. Group three: animals treated with vitamin E at a dose of 100mg/kg by intramuscular injection in concomitant with cisplatin twice weekly for one month. Animals were sacrificed and their cerebella and spinal cords were processed for light and electron microscopy. Morphometrical and statistical study was done for the mean number, as well as the mean surface area of Purkinje cells and mean surface area of their nuclei. The histological approach revealed marked degenerative changes in the Purkinje cells and motor ceurons of cisplatin treated animals [Group II]. Some of these cells appeared irregular with deeply stained cytoplasm and pykontic nuclei. Ultrastructural examination showed Purkinje cells with cellular shrinkage, damaged organelles and irregular nuclei with electron dense karyoplasms. Significant degenerative changes in the motor neurons and blood capillaries of the anterior horn of the spinal cord in the same group were frequently observed. Morphometric evaluations demonstrated significant decrease in the mean number and the mean surface area of nuclei and cell bodies of Purkinje cells. These structural and morphometrical alterations were much less observed in concomitant use of vitamin E with cisplatin [Group III]. Cerebellum and spinal cord are considered the target areas of cisplatin neurotoxicity, while vitamin E, when used in combination with cisplatin displays a protective action against neurotoxicity

Histological study on the effect of low level perinatal lead exposure on the cerebellar cortex of adult male albino rat

Lead contaminating drinking water is most often a problem in houses. As the nervous system is the primary target for the low levels of lead exposure, more attention has been directed towards lead poisoning. To determine the toxic effect of chronic low level of lead acetate on the histological structure of the cerebellar cortex of adult male albino rats. A total number of 5 pregnant albino rats were used. Lead exposure was initiated on gestation day 6 with the addition of daily doses of 0.2% lead acetate to distilled deionized drinking water and lasted until weaning. Half of the weaned male offspring were maintained on lead treated water supply until the age of two months [treated]. The remaining half received distilled deionized water until the age of 2 months [withdrawal]. Control animals received distilled deionized water. Specimens from the cerebellar cortex were processed for examination by light and electron microscope. Lead level in blood, urine and cerebellar tissue was estimated by spectrophotometry. In lead exposed rats, Purkinje cells, oligodendrocytes and Golgi cells were affected. The number of Purkinje cells decreased. The myelinated axons showed vacuoles. Blood capillaries were affected. Lead level in blood and cerebellar tissue was high. In the withdrawal group, some Purkinje cells revealed partial recovery while others showed more progress in degeneration. Chronic low level perinatal lead exposure had toxic effect on the cerebellar cortex of adult male albino rat mild regression was revealed after lead cessation

Diabetogenic effect of clozapine

Clozapine is one of the commonly used atypical antipsychotics. Several pharmacoepidemiologic studies have supported the notion that atypical antipsychotics may raise the risk of diabetes. Precise risk estimates for hyperglycemia-related adverse events in patients treated with atypical antipsychotics are not available. This study aims to clarify the diabetogenic effect of clozapine on the blood glucose level and on the cellular level by histopathological and immunohistochemical examination of pancreas. Twenty adult albino male rats were divided into two groups; first one as a control group received distilled water orally for 90 days. The other group received 13 mg of clozapine orally daily for the same duration. The rats were sacrificed and blood samples for assessment of glucose level were obtained. The pancreas was processed for histopathological, histochemical and immunohistochemical examination. The results showed hyperglycaemia in the clozapine treated group. Hisopathological examination of the pancreas of treated animals showed many large sized islets of Langerhans, sprouting of new islets from a pre-existing one and many small scattered islets within pancreatic lobules denoting hyperplastic changes. Also, some islets showed apoptotic cells and others showed lymphocytic infiltration. Endocrine-like masses of cells could be observed in relation to many interlobular ducts. Interlobular and interacinar fibrosis was observed by using masson's trichrome stain. PAS reaction revealed increased thickness of the basement membrane of the islets capillaries. Immunohistochemical staining with anti-insulin antibody showed strong staining of the hyperplastic islets of treated animals. Hislopathological and immunohistochemical observations suggested that clozapine treatment has a diabetogenic effect on the pancreatic islets of Langerhans. The pathogenesis of clozapine-associated diabetes is very similar to type 2 diabetes mellitus

Self-inflected poisoning at Assiut University Hospitals retrospective study

Suicide is a self-inflected death that is intentional rather than accidental. In the last 45 years suicide rates have increased by 60% worldwide. Deliberate self-poisoning [DSP] is the most common method of suicide in developed countries. Many substances and drugs are used; the most common are organophosphate insecticides and CNS-acting drugs. In this work a retrospective hospital-based study has been done for cases of suicidal poisoning admitted, to the emergency unit of Assuit University Hospitals from January 2004 to December 2007 were studied as regards the age group, sex, the residence, the substance used, the month of the year and the fate of cases. Statistical analysis was done for the cases. The total number of cases was 843, males represent 48.9% of them and females represent 51.1%. Using of Medications represent 46.7% of total number of cases .while Pesticides, Unknown and Miscellaneous poisons represent 29.3%, 18.5%, 5.5% respectively. The highest percentage was found among cases of age group from 15- < 25 in both males and females for all poisons. In Cities and Centers the highest percentage was recorded for medications [20.5 and 17.3 respectively], while in Villages the highest percentage was for pesticides [12.3]. The percentage of pesticides poisoning was high in June and January [14.2 and 10.9 respectively], while for medications the highest percentage was in January [13.5]. As regards the fate of cases, recovery was determined to be 70.8% of the total number of cases. Death percentage was the highest [3.8] among unknown poisons. In conclusion sex, age, residence and month of the year may have influence on suicide and the substances used for committing it

Role of nitric oxide in the pathophysiology of lead- induced cardiovascular diseases in rats

Exposure to lead is an environmental and occupational sitting continues to be a serious public health problem. Lead affects many organs and systems in human, where the cardiovascular system is one of the important targets. The mechanism of lead induced hypertension and cardiac diseases remain unclear. This study is designed to investigate the role of nitric oxide [NO] in the pathophysiologic mechanisms of lead- induced cardiovascular diseases in rats. 40 rats were used and divided into 4 equal groups. The first group was left without treatment served as a control group. The rest of groups were treated with lead acetate [0.48 mmol/L in distilled water] orally daily for 8 weeks, the third group concomitantly administered L arginine intraperitoneal injection while, the last group co administered L- N-Nitro-L arginine methyl ester intraperitoneal injection [L-NAME]. Blood samples were collected at the 4[th] and 8[th] week of the study for biochemical analysis of mean blood lead level and serum nitric oxide, lipid peroxide, total antioxidants, HDL and LDL. Measurements of systolic blood pressure were done. The mean blood lead levels, lipid peroxidation levels and LDL- cholesterol of lead treated rats were significantly higher in all groups than control. While the serum totals antioxidant levels and HDL- cholesterol significantly decreased below control levels. There was a positive correlation between mean blood lead and each of serum LDL, serum lipid peroxide and systolic blood pressure. Moreover, a significant negative correlation was observed between serum nitric oxide and each of mean blood lead, serum LDL and systolic blood pressure. These findings point to the role of nitric oxide [NO] in the pathophysiologic mechanisms of lead induced cardiovascular diseases and hypertension