1983 Volume 21 Issue 1 Pages 35-41
Male SD strain rats were subjected to 5 hr inhalation exposure to CrCl3. 6 H2O aerosol (13.3 mg Cr/m3, particle size<2 μm), killed at intervals of 1, 2 and 7 days after exposure and Cr contents in the total organ, high-molecular-weight fraction (Cr-HMW) and low-molecular-weight, Cr-binding substance (LMCr) were determined in the lungs and liver. Total Cr contents in the lungs stayed at a level approximately 8 to 25 times higher than those in the liver. Sephadex gel filtration revealed that only 3 to 10% of the total Cr was retained in LMCr in the lungs in contrast to 56 to 71% in the liver. The percentages of Cr-HMW in the total lung and liver Cr were 60 to 70% and 15 to 25%, respectively. Cr-HMW and total Cr contents in the lungs showed a slow and comparable decrease after exposure. In contrast, LMCr in the lungs gradually increased in parallel with LMCr in the liver, showing levels approximately equal to the latter. A statistically significant correlation was observed only between LMCr in the lungs and each of Cr-HMW, LMCr and total Cr contents in the liver. A linear one-compartment kinetic model gave estimates of the biological half-times of 12.8 days for lung Cr and 1.2 days for liver Cr. These results suggest that LMCr in the lungs is in equilibrium with Cr in the rest of the body and participates in the movement of Cr from the lungs to other organs. The long half-time possibly resulting in the accumulation of Cr in the lungs may be explained by the slow rate of LMCr synthesis in the lungs.
