Histomorphological changes in lung of rats following exposure to wood smoke.

Rats were exposed to repeated, intermittent exposure to smoke generated from combustion of 1g wood/15 min, total period for 75 min daily under dynamic exposure conditions, over a period of 15, 30 and 45 days. First 15 days exposure caused mild bronchiolitis, hyperplasia and hypertrophy of bronchiolar epithelial lining cells, some necrosed lining cells desquamated into lumens, congestion of parenchymatous blood vessels, oedema, hyperplasia of lymphoid follicles, peribronchiolar and perivascular infiltration of polymorphonuclear cells, and mild emphysema. These lesions progressed further during 30 and 45 days of exposure, though emphysematous changes remain constant. By 30 days and 45 days, hyperplastic and hypertrophic changes of bronchioles become quite marked, with mononuclear cells infiltration and alveolar septa thickening. Hematological studies show marginal alterations in hemoglobin levels, ESR, PCV and TLCS during 15 days, where as significant changes in eosinophil were observed during 30 and 45 days, and ESR during 45 days only. The results indicate progressive pathomorphological pulmonary lesions with subsequent exposure to wood smoke in controlled conditions.

Stage specific effect during one seminiferous epithelial cycle following ethylene glycol monomethyl ether exposure in rats.

Stage specific effect of single oral dose (500 mg/kg body wt) of ethylene glycol monomethyl ether (EGME) was characterised during one cycle of seminiferous epithelium in rats. Maximum peritubular membrane damage and germinal epithelial distortion were observed at stages IX-XII. Cell death occurred during conversion of zygotene to pachytene spermatocytes (stage XIII) and between dividing spermatocytes and step I spermatids (stage late XIII-XIV). Profound effect was noted during first meiotic division than during second meiotic division. Presence of multinucleated secondary spermatocytes indicated cytokinesis arrest. The spermatogenesis was delayed and consequently frequency of tubules at stages I-VIII was reduced by day 10. Many of the tubules were devoid of round spermatids on day 12. Possibly, EGME (or it's metabolite) distorted the barrier system at stages IX-XIV and damaged the cells mostly at stages XII-early XIV.

Distribution of mercury and evaluation of testicular steroidogenesis in mercuric chloride and methylmercury administered rats.

Intraperitoneal administration of methylmercury chloride (MMC) and mercuric chloride (MC) to male rats in doses of 5, 10 micrograms MMC/kg or 50, 100 micrograms MC/kg for 90 days induced cellular disintegration of Leydig cells which was conspicuous on day 30 and onwards in the exposed groups. Progressive degeneration of Leydig cells and decrease in their nuclear diameter and population were associated with gradual increase in deposition of mercury. Gradual diminution of 3 beta-hydroxy-delta 5-steroid dehydrogenase activity in Leydig cells after MMC or MC treatment was correlated with different structural deformations of the cells over 90 days. Moreover, a significant decrease in serum testosterone levels by day 90 confirmed steroidogenic impairment after MMC or MC treatment.

Methylmercury induced biochemical and histochemical alterations in rat testis.

The methylmercurry chloride (MMC) administered at doses of 5 and 10 micrograms/kg over a period of 90 days to male rats caused enzymatic impairments in testicular tissue. The study at intervals of 15, 30, 60 and 90 days showed gradual diminution of testicular weight and gradual decrements in testicular protein and inhibition in testicular succinic dehydrogenase activity. Histochemical and biochemical studies revealed that testicular acid phosphatase activity was also inhibited at both the doses of MMC treatment. The inhibition of enzyme activity in testicular tissues after MMC treatment caused the impairment of both spermatogenesis and steroidogenesis in rats.