[Cellular mechanisms of postnatal growth of rat liver in during chronic exposure of cadmium sulfate and strontium chloride]. / Kletochnye mekhanizmy postnatal'nogo rosta pecheni krys pri khronicheskom vozdeistvii sul'fata kadmiia i khlorida strontsiia.

A cytophotometric investigation was performed to study the ploidy level and total protein content in hepatocytes of rats of different ages (1, 7, 14, 21, 30, 90, 180, 365 days), both intact and chronically treated with cadmium sulfate or strontium chloride. It was established that during the first month of postnatal ontogenesis, compositions of liver parenchyma cell population of intact and treated rats did not differ. Compared to control animals, the process of cell polyploidization in the liver of rats treated with heavy metal salts of 30-90 days proceeded slower, especially in Cd(2+)-treated rats. Within 180-365 days the cell polyploidization in the treated animals increased. The proportion of (4c x 2)-hepatocytes in 1 year old Cd(2+)- or Sr(2+)-treated rats increased, resp., by 2.7 and 1.5 times, and that of 8c hepatocytes was higher by 3.9 and 1.5 times than in the control, the average ploidy level rising by 20 and 5%. respectively. It was established that until 90 days the rate of protein accumulation in liver cells of intoxicated rats was slower than in intact animals. Thus, the average protein content per diploid hepatocyte in Cd(2+)- or Sr(2+)-treated 30 day old rats was lower by 20 and 16%, respectively, compared to control animals. The protein content increased in liver cells of Cd(2+)- or Sr(2+)-intoxicated rats following 90 and 180 days, respectively, and this process was exclusively associated with cell polyploidization. During the first 3 weeks after birth, no significant difference was observed in the extent of involvement of cell proliferation, polyploidization and hypertrophy in the growth of liver in intact and intoxicated animals. At this period the liver was growing due completely to cell proliferation and hypertrophy. During 21-30 days the contribution of cell proliferation to the liver growth of intact rats was not significant (29%), whereas it remained at higher level (50%) in the treated animals. In 30-90 days after birth, the involvement of proliferation process to the liver growth of intoxicated rats decreased to 25-28%, while in intact animals it increased up to 37%. At this period the cell polyploidization plays an essential role in the growth of liver in both intact and intoxicated animals to reach in average 37-46%. The contribution of polyploidization and hypertrophy to the liver growth of Cd(2+)-treated rats within 30-90 days was obviously higher than in Sr(2+)-treated animals. Both at the late (3-12 months) and at the early (1-21 days) stages of experiments, the pattern of correlation of different cell components in the growing liver of intact and intoxicated rats differed only a little.

[Effect of cadmium sulfate and strontium chloride on the glycogen content in hepatocytes of rats of various ages]. / Vliianie sul'fata kadmiia i khlorida strontsiia na soderzhanie glikogena v gepatotsitakh krys raznogo vozrasta.

Cytophotometry and image analysis being used, hepatocyte glycogen contents were measured in periportal and pericentral zones of liver lobules at different stages (1, 7, 14, 21, 30, 90, 180 and 365 days) of postnatal development of both intact rats and rats exposed to chronic CdSO4 (1 mg/kg body weight) and SrSO4 (6.5 mg/kg body weight) intoxication. The glycogen content in hepatocytes of intact rats increased continuously in the course of development being most highest at the initial stage of development. The glycogen content ratio in cells of portal and central zones of liver lobules varied during ontogenesis. The maximum value of this ratio is reached on the 21st day after the rat birth, dropping sharply at later age to reach its minimum in adults. Intoxication of rats by Cd2+ and Sr2+ within 1-90 days interval reduced hepatocyte glycogen levels, compared to normal liver. The prolongation of rat treatment with heavy metals for 90-365 days led to glycogen accumulation in hepatocytes. Rat intoxication with heavy metals for 1 year brought about the increase in both glycogen content per cell and glycogen concentration. Cd2+ treatment for 30-90 days resulted in glycogen accumulation inhibition in both the investigated zones of liver lobules. Thereafter an increased glycogen accumulation took place in hepatocytes of the portal and central liver lobules. Following Cd2+ treatment, the value of the ratios of glycogen levels in the portal and central liver lobules was lower than in the normal liver on all stages of the postnatal rat development. The lowest value (< 1.0) of this ratio was reached in the cirrhotic liver. Distinct from Cd2+ treatment of rats, the treatment with Sr2+ does not lead to significant changes in glycogen levels in cells of different zones of liver lobules. Nevertheless certain destructive changes in glycogen-forming function of hepatocytes after Sr2+ treatment are apparent. This is suggested from the lower glycogen levels in the portal and central zones of liver lobules on 30-180 days interval compared to the normal liver. Besides, the values of ratios in glycogen levels in the portal and central zones of liver lobules in 14 and 21 days old rats was noticeably lower than in the intact rats of the same age.