ABSTRACT
Exposure to air pollution is associated with increased respiratory and cardiovascular morbidity, although the underlying mechanisms are unclear. Thus the way of assessing the effects of inhalation of whole mixtures from defined sources as tobacco smoke and car exhaust need lobe considered more. To investigate using histological, histochemical, immunohistochemical and morphometric study, the harmful effects of tobacco smoke and car exhaust on adult male albino rats' lung and the influence of arrest of these air pollutants. Thirty adult male albino rats were randomly divided into three groups: control group, tobacco exposed group, and car exhaust exposed group. Rat's general condition and behavior were noticed and they were weighed at the beginning of research and at the time of sacrific, Paraffin sections were prepared for histological, histochemical, immunohistochemical using marker CD44 and morphometric study and statistical analysis were done. Rats exposed to tobacco smoke or car exhaust showed significant decrease in body weight more intensified after car exhaust which remained significantly less than control rats after arrest of exposure. Histological. histochemical, immunohistochemical and morphometric changes were more exaggerated after car exhaust than after tobacco exposure. Rats showed pulmonary congestion, extravasation of blood in lung alveoli, perivascular infiltration and thickened interalveolar septa, obliteration of most alveoli and subsequently compensatory emphysematous changes. There was increased deposition of collagen fibers and apparent increase in niucopolysaccharides and immunohistochemical reaction CD44. Arrest of exposure to either tobacco smoke, or car exhaust caused partial recovery which was less ameliorated after car exhaust. These results provide evidence that air pollution from either tobacco smoke or car exhaust are risky factors for parenchymal lung damage and marked thickening of the interalveolar walls. Partial recovery was observed after arrest of tobacco smoke better than after car exhaust
ABSTRACT
Acetyl salicylic acid [Aspirin] is almost the most widely used drug both therapeutically [to reduce pain, inflammation and fever] and prophylactically [to prevent thrombotic events]. Aspirin [ASA] represents an important risk factor for gastric mucosal injury. The roles of active oxygen metabolites and anti-oxidative defenses in aspirin [ASA]-induced gastric damage and their amelioration still needed to be clarified. Vitamin C is an ideal antioxidant to increase tissue protection due to its easy, effective and safe dietary administration in large range of concentration without harmful side effects. To investigate through histological examination by light and electron microscope and morphometric study the effects of aspirin with or without ascorbic acid [Vitamin C] for 2 weeks on fundic mucosa of adult male albino rats. Twenty eight adult male albino rats were used and randomly divided into four equal groups: Control group; vitamin C group was given 200 mg/kg body weight; ASA group was given 100 mg/kg body weight of aspirin; the fourth group was given both vitamin C and aspirin. Animals treated daily for 2 weeks then sacrificed by cervical dislocation. Stomach tissues were excised for macroscopic, light and electron microscopic study and morphometric analysis. Oral administration of aspirin induced marked changes in gastric mucosa detected by both light and electron microscope ranging from simple hemorrhagic streaks to marked damage with severe erosions, exfoliation and presence of wide areas of epithelial discontinuity [ulcer formation]. This was accompanied by significant decrease in the count of lining cells except parietal cell count. Ulcer Index [UI], showed high significant increase. The addition of vitamin C significantly attenuated gastric damage and could protect gastric mucosa against the injurious effect of aspirin as evidenced from decreased UI and parietal cell count together with restoration of mucosal appearance. These results concluded that ASA combined with vitamin C in comparison with ASA induced less gastric mucosal damage and this protective effect might be due to the attenuation of oxidative stress and decreased count of parietal cells and consequently decrease of gastric acidity