ABSTRACT
BACKGROUND: Acrylamide (ACR) exposure is associated with neurotoxicity, carcinogenicity, and reproductive toxicity. The use of soy sauce as a condiment is common and it has been found that it possesses high antioxidant activity. The objective of the current study is to evaluate the protective role of dark soy sauce (DSS) against ACR-induced neurotoxicity in rats. MATERIALS AND METHODS: Thirty-five adult male rats were divided into four groups: control, ACR given for 4 weeks, DSS given for 4 weeks before ACR, and DSS given with ACR for 4 weeks. The trigeminal ganglia and cerebellum were dissected and processed for histological staining with haematoxylin and eosin and immunohistochemistry for synaptophysin (SYP) and morphometric analysis. RESULTS: In the trigeminal ganglia, ACR group showed central chromatolysis, degeneration and cell loss. DSS before ACR group had less marked changes in the neuronal architecture, while in ACR with DSS group, better preservation was observed. In the cerebellum, ACR group showed shrunken Purkinje cells and nuclear pyknosis. Spacing and dissociation between Purkinje layer and other layers was seen. DSS before ACR group showed few degenerated Purkinje cells with normal pattern of the other layers of cerebellar cortex. ACR with DSS group showed less disturbed cerebellar layers architecture. Cerebellar SYP immunoexpression and its area per cent were decreased in ACR group compared with the control. It increased in both DSS treated groups, specifically DSS concomitantly given with ACR. CONCLUSIONS: ACR exerted marked cellular degenerative effects and administration of DSS and ACR at the same time had neuroprotective effect. DSS treatment before ACR exposure gave only marginal improvement.
ABSTRACT
BACKGROUND: The moisture content of diet and the dryness of the mouth alter the volume of parotid saliva secreted in rats and it plays an important part in mastication and swallowing. Temporary or permanent liquid diet feeding provides a nutritional regime for patients in certain medical situations. The aim of the present work is to investigate the sequel of liquid diet on parotid gland in rats and the possible protective role of L-carnitine (L-car). MATERIALS AND METHODS: Thirty adult male albino rats were divided into three groups (10 per group) - CONTROL GROUP: rats were fed on regular pellet diet, Liquid diet group and Liquid diet supplemented with L-car group were received liquid diet. The parotid glands were dissected for histological, immunohistochemical and ultrastructural analysis. RESULTS: By light microscope, liquid fed group showed some areas with degenerated irregularly shaped acini and atrophic acini with vacuolated cytoplasm and pyknotic nuclei. Acinar cells of parotid gland group on liquid diet supplemented with L-car, had normally eosinophilic cytoplasm with few vacuoles in their acinar cells. Periodic acid Schiff (PAS) staining, in liquid fed group showed that the serous acini were weakly stained with PAS that was localised in the apical portion of the cells where the secretory granules lie with lack of staining of the vacuoles. However, moderately stained acinar epithelial cell and fewer vacuoles was seen in group given liquid diet supplemented with L-car. Immunohistochemistry of Caspase 3 showed more apoptotic cells with increased area per cent of Caspase 3 immunoexpression, seen in the acini and more in the ductal epithelium in liquid fed group. It was markedly reduced in the acinar cells in group on liquid diet supplemented with L-car. Electron microscopic study revealed in liquid fed group acini with multiple cytoplasmic vacuoles and reduced secretory granules, degenerated swollen mitochondria and dilated cisternae of endoplasmic reticulum. Degenerated condensed nuclear mass or indented nuclear membrane, nuclei with karyorrhexis and chromatin material leaked in the cytoplasm with rupture of the nuclear membranes were also seen. In parotid gland of liquid fed group supplemented with L-car, acinar cells showed normally distributed secretory granules and few cytoplasmic vacuoles. They showed normal appearance of the nuclei and their cytoplasmic organelles. CONCLUSIONS: Liquid diet caused cellular degenerative damages and apoptotic changes in parotid gland and these changes can be prevented by L-car supplementation probably by its antioxidant properties.
ABSTRACT
BACKGROUND: Bisphenol-A (BPA) is an industrial chemical, used to manufacture polycarbonate and numerous plastic articles. It has been found to cause biological effects, mimic that of oestrogen. It belongs to a group of chemicals termed "endocrine disruptors" able to disrupt the chemical messenger system in the body. Aim of the study was to demonstrate the biological effects of BPA on the vagina of female rats, with the prediction of the neoplastic changes in relation to its potential impact. MATERIALS AND METHODS: Sprague-Dawley gravid dams were divided into three groups (10 per group): G1 - control group had an equivalent volume of sesame oil to that taken in the treated groups, G2 - group was administered by gavage 0.1 mg BPA/kg body weight (low-dose group) per day, and G3 - group was administered 50 mg BPA/kg body weight (high-dose group) per day, dissolved in sesame oil. Treatment was carried out on gestation days 10 through 20. The female offsprings of each group were weaned at day 21 and the vagina was dissected when became 3 months old for histological, immunohistochemical analysis (for detection of oestrogen receptors a [ERa], and the proliferation marker Ki-67), and ultrastructural study. RESULTS: The low dose group showed degeneration of the epithelial lining with focal patches of decreased epithelial layers. The high dose group revealed cytoplasmic hydropic degeneration, and the pyknotic nuclei of epithelial cells. Oestrogen receptors demonstrated a significant decrease of positive cells in low dose treated group and this decrease markedly accentuated in the high dose one. Positive nuclei for Ki-67 were markedly increased with increasing doses of BPA. Electron microscopic study revealed cytoplasmic degeneration, vacuolation and mitochondrial degeneration in both treated groups. CONCLUSIONS: BPA showed an obvious mix of degenerative and proliferative histological changes and clear damage of the cellular organelles. This stressful condition may predispose to neoplastic changes of the vagina.
ABSTRACT
BACKGROUND: Sertoli cells are important in determining the fate of spermatogenic cells by providing nutrition and structural support via cell junctions. Adhesion between Sertoli and germ cells is important for spermatogenesis. Cadherin are transmembrane proteins that mediate cell-cell adhesion, while, vimentin, the cytoskeletal intermediate filament plays an important role in spermatogenesis. The aim of the present study was to investigate cadherin and vimentin immunoexpression in the normal testis and in two types of altered spermatogenic states: the cyclophosphamide (CP) treatment and the cryptorchidism (Cx) models. MATERIALS AND METHODS: Twenty four male albino rats were divided into control group: 6 rats receiving saline orally and the other 6 were sham-operated. CP group (n = 6): given 6 mg/kg/day of CP orally for 4 weeks. Cx group (n = 6): the left testis was surgically freed from the scrotum and fixed in the abdomen. Animals were sacrificed and the left testis dissected and prepared to be stained with haematoxylin and eosin stain and immunohistochemical stain against cadherin and vimentin. Morphometric measurements and statistical analysis were done. RESULTS: In CP-treated group there was degeneration of spermatocytes, vacuolations of Sertoli cells and absence of spermatozoa. These changes were more prominent in Cx group, in addition to interstitial hypercellularity. There was alsoa significant decrease in cadherin and vimentin immunostaining in CP-treated group that was more marked in the cryptorchidism group. CONCLUSIONS: A downregulation of both cadherin and vimentin was associated with both models of impaired spermatogenesis. This impairment could be attributed to disruption of the junctions between Sertoli and germ cells.
