The correlation between age and serum β2-MG levels and between age and urinary β2-MG levels of Japanese was studied, and the results were as follows. 1. The correlation coefficients between age and β2-MG level in the serum were +0.240 for males, +0.448 for females and +0.303 for both sexes. 2. The correlation coefficients between age and actual β2-MG level in the urine were +0.321 for males, +0.294 for females and 0.288 for both sexes. 3. The correlation coefficients between age and β2-MG level corrected for creati-nine in the urine were +0.265 for males, +0.423 for females and +0.345 for both sexes. 4. The correlation coefficients between age and β2-MG level corrected for density in the urine were +0.278 for males, +0.315 for females and +0.298 for both sexes. 5. The correlation coefficients between cadmium level and β2-MG level in the urine were +0.075 for males, +0.618 for females and +0.441 for both sexes. 6. The correlation coefficients for items (1) to (5) were significantly different from zero (p<0.05).
Effect of chlorobenzene administration on glutathione metabolism in rat liver was investigated. Rats were intraperitoneally injected with chlorobenzene (2.0 mmol/kg). At 6 hours, hepatic total and oxidized glutathione in the rat with chlorobenzene decreased to 24% and 53% of those in control rats without chloro-benzene, respectively. When 24 hours passed after the injection, the total and oxidized glutathione increased to 188% and 170% of the control, respectively. And simultaneously, the activities of hepatic glutathione synthesis and glutathione reductase elevated to 193% and 136% of the control, respectively. At 48 hours, these elevation were still found and the liver was enlarged with significant increase in the protein and DNA. The activities of hepatic γ-glutamyltranspeptidase and glutathione peroxidase were unaltered by the chlorobenzene. Similarly to the single injection, four times intraperitoneal injection with chlorobenzene (2.0 mmol/kg/one shot at 48 hours-intervals) caused the hepatic enlargement and the accumulation of hepatic glutathione. These results indicate that the acceleration of hepatic glutathione synthesis, occurring in response to the transient decrease of glutathione, caused the accumulation of glutathione in liver of rat injected with chlorobenzene.
This study was undertaken to predict the neurochemical effects of two environmental factors simultaneously. Guinea pigs were exposed alternately to SO2 (10 ppm) and H2S (20 ppm) one hour daily for 30 days. Combined toxicity of SO2 and H2S revealed statistically significant decrement of the total lipids in all the regions of the brain and spinal cord. A significant decrement was also discernible in the levels of phospholipids in the cerebral cortex and spinal cord.While, phospholipids concentration was significantly elevated in cerebellum and in the brain stem. The contents of cholesterol exhibited remarkable depletion in all the regions of the brain and spinal cord. In spite of varied responses of cholesterol and phospholipids, C/P ratio showed decrement in various regions of the brain and spinal cord. The concentration of free fatty acids exhibited increment in cerebral cortex and basal ganglia, but the cerebellum, brain stem and spinal cord showed decrement. Remarkable diminution in the concentration of esterified fatty acids was discernible in cerebral cortex, cerebellum and in the spinal cord. Interestingly, these levels showed significant elevation in the brain stem. On the other hand, the concentration of gangliosides showed a significant increase in basal ganglia, cerebellum and in the brain stem. However, these levels were significantly decreased in the cerebral cortex. Lipid peroxidation and lipase activity showed remarkable elevation in different regions of the brain and spinal cord. The results clearly show that peroxidation of endogeneous lipids has been enhanced by SO2 and H2S and thus led to degradation of brain lipids. However, lipid fractions have exhibited regional heterogeniety.
Studies were made on the usefulness of measureing the fluoride con-centration in the serum and urine as an index for the health care of hydrofluoric acid (HF) workers, particulary for those with diminished renal function. Renal clearance of fluoride (CF), the amount of fluoride filtered by the glomeruli per minute (FF) and tubular reabsorption of fluoride (TrF), which were calculated from the serum concentration, as well as the quantity concurrently excreted in the urine and the glomerular filtration rate (GFR), were investigated in patients with chronic renal failure (CRF) and healthy controls after the oral administration of sodium fluoride (as 4 mg F-) with water loading. After the administration the 24-hour excretion of fluoride in the patients with CRF was significantly lower (p<0.0.01) than controls. CF, FF, and TrF were also lower in the patients. CF and creatinine clearance (Ccr) were well correlated (r= +0.87) with CF averaging 48% of the Ccr. Elevated concentrations of fluoride were observed in the serum of patients with CRF and HF workers. Three HF workers who had clinical evidence of renal failure showed a higher level of serum fluoride. However, their urinary level of fluoride showed normal values. The results showed that the urinary excretion of fluoride decreased with the reduction of renal function. Moreover, compared to urinary levels the fluoride concentration in the serum may be a more direct indicator of exposure in patients with kidney hypofunction.