ABSTRACT
Nicotine neuronal interactions exert an adverse potential in some brain regions and a significant link has been established between tobacco smokeicotine and vascular impairment. This work addresses nicotine impact on various components of the substantia nigra compacta (SNc) in rat. Twenty adult male Albino rats were divided equally into two groups: Group I, vehicle-control group (received saline [1 ml/kg body weight intra peritoneally] for 11 days). Group II; nicotine group (received 1.5 mg/kg body weight/day Sc) for 11 days. Nicotine levels were detected in the serum. Specimens were taken from the mid brain, processed and examined using biochemical, immunohistochemical, ultrastructural and morphometric techniques. In nicotine group, biochemical analysis revealed reduction in total antioxidant capacity (TAC), decrease in dopamine and malondialdehyde (MDA) levels. The mean number of light cells, and the mean surface area of nerve cells/field were significantly reduced, with an increase of dark cells were found in nicotine group compared to control.Immunoreactivity in nicotine group revealed an increase in neuronal α-synuclein, reduction in tyrosine hydroxylase enzyme, an increase in caspase 3 and ultrastructure changes suggestive of neuronal apopto. The blood capillaries were markedly affected. Nicotine induced endothelial and pericytic apoptotic changes, irregular lumena and indistinct endothelial junctional complex. Nicotine administered subcutaneously in a small dose may have a deleterious effect on SNc, mainly involving dopaminergic neurons and blood capillaries. This effect seems to be secondary to an oxidative stress that might be produced by reduced TAC and increased MDA levels.
ABSTRACT
Nicotine neuronal interactions exert an adverse potential in some brain regions and a significant link has been established between tobacco smokeicotine and vascular impairment. This work addresses nicotine impact on various components of the substantia nigra compacta (SNc) in rat. Twenty adult male Albino rats were divided equally into two groups: Group I, vehicle-control group (received saline [1 ml/kg body weight intra peritoneally] for 11 days). Group II; nicotine group (received 1.5 mg/kg body weight/day Sc) for 11 days. Nicotine levels were detected in the serum. Specimens were taken from the mid brain, processed and examined using biochemical, immunohistochemical, ultrastructural and morphometric techniques. In nicotine group, biochemical analysis revealed reduction in total antioxidant capacity (TAC), decrease in dopamine and malondialdehyde (MDA) levels. The mean number of light cells, and the mean surface area of nerve cells/field were significantly reduced, with an increase of dark cells were found in nicotine group compared to control.Immunoreactivity in nicotine group revealed an increase in neuronal α-synuclein, reduction in tyrosine hydroxylase enzyme, an increase in caspase 3 and ultrastructure changes suggestive of neuronal apopto. The blood capillaries were markedly affected. Nicotine induced endothelial and pericytic apoptotic changes, irregular lumena and indistinct endothelial junctional complex. Nicotine administered subcutaneously in a small dose may have a deleterious effect on SNc, mainly involving dopaminergic neurons and blood capillaries. This effect seems to be secondary to an oxidative stress that might be produced by reduced TAC and increased MDA levels.
ABSTRACT
Malathinon is an organophoshorus insecticide [OPI] widely used in agriculture to disinfect crops and stored gains and in some medicine to treat lice and scabies. In this way it can reach to general population and not only to persons working with it. Malathion low dose is toxic to many organs/system of the body and it has been observed that oxidative stress may have a role in malathin toxic action. Many researches have been done on its effect on male genital system. Meanwhile studies on the female reproductive system especially the ovary are limited and need further investigation. Is to the effect of chronic exposure to malathion on the ovary and the role of vitamin C in ameliorating the possible changes induced by malathion. A total number of 70 young adult female rats were used divided into three groups. Group I: 10 animals were kept as control groups. Group II: 30 animals treated with malathion at a dose of 100 mg/kg/day by intragastric tube for two months. Group III: 30 animals treated with vitamin C in a dose of 20 mg/100gm/day given two hours earlier before the dose of malathion for two months. Animals were sacrificed and their ovaries were processed and examined using histological and immunohistochemical [PCNA and Caspase 3] and morphometric techniques. After malathion treatment. The ovary showed significant decrease in the number and size of various types of follicles associated with a significant increase in the atretic follicles. Oocytes looked shrunken with irregular ZP and ill defined nucleolus. Immunohistochemically, there was an increase in the intensity of caspase 3 [maker of apoptosis] reaction and decrease in the PCNA [maker for cell proliferation] immunostaining. Treatment with vitamin C as antioxidant showed some improvement in the ovary. Malathine induced direct ovarian damage that will affect the fertilitry and the coadministration with vitamin C can partially ameliorate these changes. So it is not completely protective
Subject(s)
Female , Animals, Laboratory , Ovary/pathology , Histology , Immunohistochemistry , Protective Agents , Ascorbic Acid , Treatment Outcome , Rats , FemaleABSTRACT
Fluoride accumulation in the brain of experimental animals was particularly observed in the hippocampus. It caused altered neuronal and cerebrovascular integrity, abnormal behavioral patterns and metabolic brain lesions. Fluoride affected indeed the cerebellar development in mice but its effect on adult rat cerebellar cortex is something awaits further investigation. Is to define the effects of fluorosis on the histological structure of adult rat cerebellar cortex. A total number of 40 adult female albino rats were used. They were divided into two groups [20 animals each]. Group I: Was kept as control group, received distilled water orally daily by gastric tube for 2 months. Group II: Received sodium fluoride orally [dissolved in distilled water] at a dose of 12 mg/Kg body weight for two months. Samples from cerebella were taken and processed for light and electron microscopic investigation. After fluoride treatment, features of neurodegeneration were observed. The Purkinje cells appeared shrunken, deeply stained, with multilayer disposition, which was confirmed by morphometric evaluation of the Purkinje cell layer thickness. Ultrastructurally, increased infolding of nuclear envelope, mitochondrial alterations, dilated Rough endoplamic reticulum cisternae and clusters of vesicles near the Golgi bodies were observed. Apoptotic granule cells accumulated in a clumping manner, Bergmann astrocytes with features of increased activity, dilated and congested blood capillaries were noticed. GFAP positive cells were more abundant and appeared larger in the three cortical layers of treated animals associated with positive reaction for inducible nitric oxide synthase [iNOS] compared to negative reaction in control animals. The cerebellar cortex was particularly susceptible to sodium fluoride- induced oxidative stress and could contribute to the development of neurodegenerative diseases
ABSTRACT
Reticular or net-like perineuronal coatings, termed perineuronal nets [PNs], enriched with proteoglycans [PGs] and/or glycoproteins [GPs] were demonstrated to ensheath cell surfaces of certain neuronal circuits in the central nervous system of mammals, reptiles and fishes. In this investigation, three types of coated neuronal circuits were histochernically demonstrated in the adult rat retrosplenial cortex [RSC]; PGs-, GPs- and PGs/GPs- coated neuronal types. The PGs coated neurons were histochemically detected with a cationic iron colloid [CIC] staining or CIC/Bodian enhancement procedure. The GPs coated ones were detected with certain plant lectins from Vicia villosa agglutinin VVA Wisteria florihunda agglutinin WFA or Glycine max agglutinin SBA for N-acetylgalactosamine-binding. The netassociated neurons were mostly distributed throughout the cortical layers II-V Their mean number per UA [60.15 micro M[2] was ranged from 9.87 +/- 0.43-10.50+2.61 in 8-month old rat and forming about 24-26% of total neuronal population. Statistical Analysis revealed that the mean numbers of PGs, GPs and PGs/GPs coated cells were 0.84 +/- 0.07, 6.33 +/- 0.34 and 2.70 +/- 0.22, respectively. Their percentages represented about 9%, 64% and 27% of total coated neurons in RSC, respectively. Notably, the labeled retrosplenial neurons underwent a non-significant increase in number with progression of age during the first post natal year; however, they declined thereafter toward senility. This data indicated that the extracellular matrix of net- associated retrosplenial neurons in adult albino rat was enriched with GPs and/or PGs molecules and this neurochemical heterogeneity might have diverse biological and functional properties of the neurons in RSC