Tocopherol Enhances the Antioxidant Defense System and Histomorphometric Parameters in The Gastrointestinal Tract of Rats Treated with Sodium Arsenite.

Arsenic compromises the gastrointestinal integrity and function via the body's anti-oxidative system breakdown.  Hence, this study aimed to investigate the effects of tocopherol on redox imbalance and histoarchitectural alterations in rats' gastrointestinal tract exposed to sodium arsenite. Sodium arsenite and graded doses of tocopherol were administered orally into experimental rats assigned to different groups for four weeks concurrently. Redox status assay was done in homogenized samples by spectrophotometry. Parietal cell mass and mucous cell density (stomach), villus height and crypt depth (ileum), goblet cells count, and crypt depth (colon) were evaluated by histomorphometry. Inflammatory cells infiltration was also assessed using a semi-quantitative procedure. Sodium arsenite caused a significant increase in Malondialdehyde and Myeloperoxidase but, decreased Superoxide dismutase, Catalase, Nitric oxide, Glutathione peroxidase, Glutathione, and Glutathione-S-Transferase. Tocopherol treatment reversed the changes (p<0.05) though not largely dose-dependent. Furthermore, tocopherol annulled sodium arsenite-induced increase in parietal cell mass and decrease in mucous cell density in the stomach, decrease in villus height and villus height/crypt depth ratio in the ileum, and decrease in goblets cells and increase in crypt depth in the colon. Moreover, activated inflammatory cell infiltration by sodium arsenite was mitigated by tocopherol. Sodium arsenite provokes not only marked inflammatory cellular infiltration but a focal loss of glands, hyperplasia of crypts, atrophic villi, and hypertrophy of Peyer's patches in the intestines, which are all lessened with tocopherol treatment.  These findings underscore the anti-oxidative properties of tocopherol as a potent dietary factor against sodium arsenite toxicity in the gastrointestinal tract. Keywords: Tocopherol, arsenic, stomach, ileum, colon.

Standardized experimental model for cement dust exposure; tissue heavy metal bioaccumulation and pulmonary pathological changes in rats.

A controlled experimental model of exposure to aerosols particularly for cement dust was recently invented in a study from the laboratory that found high serum levels of heavy metals, decrease gastrointestinal motility, and altered hematological variables in cement dust exposed rats. However, reproducibility was not considered. This work aims at standardizing the model and investigating preliminary toxicological indicators. Thirty male rats used in this study were divided into 3 groups (n = 10). Group 1; control, while groups 2 and 3 were exposed to cement dust for 14 days and 28 days respectively. We assessed clinical signs of toxicity, tissue heavy metal concentration, histopathological, and body weight (BW) changes. We observed poor movement coordination, abnormal posture, cephalic fur loss. Evidence of ischemia and fibrotic pneumoconiosis were grossly observed in the lungs of the exposed groups. There was a significant increase in tissue level of heavy metals with pulmonary and gastric heavy metal content showing a trendy relationship during the period of the exposure as the value of Lead, Chromium, Cadmium, Iron, Calcium, and Nickel increased by nearly similar percentages in both tissues. Organs weights increased; the 14-day exposed (198 ±â€¯31; 168 ±â€¯22) and 28-day exposed (198 ±â€¯22; 187 ±â€¯26) groups had significantly reduced body weight at the first and second weeks of exposure compared to the control group (265 ±â€¯26; 357 ±â€¯40) respectively. Exposure to cement dust induced low bone density in the exposed rats (p < 0.05). Histopathological alterations include necrosis, inflammatory cellular infiltration, and alveolar hyperplasia suggestive of the proliferative response of pulmonary tissue to the dust. The operation of the standardized apparatus mimics a typical occupational exposure and the findings show that cement dust induces systemic toxicity via respiratory perturbation and body/organ weight discordance mediated by heavy metal bioaccumulation.