possible protective effect of vitamin C on the kidney cortex of adult female albino rat after chronic exposure to malathion: a light and electron microscopic study

Chronic exposure to malathion is still a major medical problem in occupational and environmental settings. The raised issue of the antioxidants effect on different tissues provides a new line of protection against the inevitable exposure to insecticide residues in food or through environmental contamination. The aim of the study was to determine the effects of vitamin C supplementation on renal cortical tissue after chronic exposure to malathion. Thirty female albino rats aged 3 months were divided into three equal groups: group I control adults were fed the basal diet; group II was given commercial malathion dissolved in distilled water orally by intragastric tube at a dose of 100 mg/kg/day for 2 months; and group III was given malathion in the previously described way at the same dose in addition to vitamin C [pure ascorbic acid powder] dissolved in distilled water and given orally by intragastric tube at a dose of 20 mg/100 g/day for 2 months. The specimens were obtained from the kidney and prepared for light and electron microscopic examinations. Morphometric and statistical studies were carried out in the three studied groups. It was observed that treatment with malathion disrupted the normal histological structure of the renal cortex. Thickened glomerular basement membrane was evident. There was widespread vacuolation of tubular lining epithelium and increased heterochromatin clumps in most of the nuclei. The mitochondria appeared disorganized with loss of cristae. The diameter of renal corpuscles and renal tubules increased, whereas tubular epithelium height decreased significantly compared with the control. Moderate improvement in the previous findings was detected on concomitant supplementation of vitamin C. Vitamin C supplementation played a protective role on the renal cortex exposed to chronic malathion toxicity at the subcellular level

Histological study of megakaryocytogenesis and thrombocytogenesis in the guinea pig bone marrow with reference to the role of adipocytes

Blood platelets play a pivotal role in hemostasis and participate directly in thrombosis and atherosclerosis. The aim of the study was to investigate the steps of platelet production, the morphological changes that occur during proplatelet production, the cytoskeletal mechanics that drive these transformations, and the possible role of stromal cells in platelet formation. Red bone marrow fragments were harvested from ten adult male guinea pigs. Toluidine blue-stained semithin sections were prepared for light microscopic examination, and ultrathin sections were examined by transmission electron microscope. In the semithin sections of the bone marrow, nearly half of the area contained hematopoietic cells, whereas the remainder was occupied by adipocytes that showed unusual bridging connections between them. In addition, the megakaryocytic lineage cells assumed a unique close association with the neighboring adipocytes. Under transmission electron microscope, the surface of the immature megakaryocytes was characteristically smooth, whereas mature megakaryocytes developed characteristic proplatelets in the form of coarse surface cytoplasmic processes that bulged to the outside and detached as preplatelets. Granules and membranes associated with microtubules were translocated from the base of proplatelets to appear in their cytoplasm, and the invaginated membrane system became extensive in the mature megakaryocytes. Sometimes, these cells extended large proplatelets through the attenuated sinusoidal walls, where they discharged preplatelets that further fragmented into platelets. The formation of proplatelets and the elaboration of granules into the newly formed preplatelets and platelets were largely dependent on the efficiency of microtubular cytoskeletal elements. Marrow stromal cells, especially adipocytes, might be involved in megakaryocytic lineage development

Ultrastructural intestinal pathology induced by human Blasocystis in experimentally infected mice

Blastocystis spp. is a single-celled anaerobic enteric parasite that inhabits the lower gastrointestinal tract of humans and many animals. This emerging parasite with a worldwide distribution is often identified as the most common eukaryotic organism reported in human fecal samples that showed a dramatic increase in recent years; however its pathogenicity still shows many contradictions. To evaluate the histological and ultrastructural pathological changes induced by human Blastocystis isolates in the intestine of experimental infected mice. Fecal samples positive for Blastocystis were collected from patients, and processed for culture using Jones' medium. Cultured samples were subjected to examination by light and transmission electron microscopy. Blastocystis cyst stages were isolated and orally fed to immunocompetent BALB/c mice. Mice were sacrificed 2 weeks post infection. Semi-thin and ultra-thin sections prepared from their intestine were examined by both light and transmission electron microscopy [TEM], respectively. Blastocystis showed different forms: vacuolar, granular, amoeboid and cysts within 24 hours in culture. Histological examination of infected intestine showed vacuolar, granular and amoeboid forms in the caecum, but only cyst forms were observed in the colon. Intense inflammatory cell infiltration, edematous lamina propria, and villous atrophy were noticed. Ultrastructure of Blastocystis hominis by TEM revealed the surface coat with outer fibrillar layer, nuclei with multiple chromatin masses, and mitochondria with some pathological tubular changes. Atrophy and sloughing of microvilli of infected intestine was noticed in comparison to the mucosa of control non-infected mice that showed normal brush border and microvilli. Infection with Blastocystis may be self limited in some hosts however it may cause considerable pathological changes such as enterocytes invasion and intestinal mucosal atrophy of infected mice. Blastocystis mitochondrial vacuolations were detected within intestine of infected mice compared to culture forms. Thus, apparently B. hominis is capable of causing pathogenicity