Abstract: The urinary concentration of cadmium, copper and zinc was deter-mined in 12 male workers who had been engaged in welding work with cadmium-containing silver solder. Sephadex chromatographic analysis for these urinary metals was performed in two workers suspected of suffering cadmium-induced renal injury. The mean values of the cadmium, copper and zinc concentrations in the urine of the welders were about 26, 2.4 and 2.6 times the control values, respec-tively. A linear relationship was obtained between the urinary concentrations of cadmium and both copper and zinc. The chromatographic distribution of these urinary metals in the welders showed that the metallothionein fraction contained cadmium and copper, but not zinc. The copper content of this fraction was much larger than the cadmium content. The cadmium and copper in this fraction repre-sented about 6% and 10% of the respective total amounts of these metals in the urine. The remaining cadmium and copper were recovered from the high molecular weight protein fraction and low molecular weight nonprotein fraction. The urinary zinc was recovered from both these fractions. The zinc in the latter fraction represented 85% of the total urinary zinc. The present results suggest that cadmium accumulation affects the excretion of copper and zinc in the urine, and that the urinary excretion of metallothionein containing cadmiun as well as copper may be involved in cadmium induced renal injury.
Present experiment was performed on twenty laboratory-bred female squirrels (Funambulus pennanti, Wroughton). The animals were divided into 2 groups: (1) Cd-treated and (2) control. A single intraperitoneal injection of cadmium acetate (6 mg Cd/Kg of body weight) was given in each animal except the animals of control group. The animals were sacrificed by decapitation after different intervals of the week long study. Ovary and uterus did not show any histopathological abnormality after cadmium exposure. Whereas, the animals of the two groups revealed increase in body weight, i.e. 1.15 folds (control) and 1.03 folds (Cd-treated). It is suggested that ovary and uterus could not be affected by acute cadmium exposure possibly because the enzymatic activity could not be disturbed or inhibited in these organs.
Respiration and oxidative phosphorylation in rat liver mitochondria were investigated by the oxygen electrode method, and the livers of rats administered with polychlorinated naphthalene at 500 and 1000 mg/kg of food for 90 days were examined. A high dose of polychlorinated naphthalene given by intraperitoneal injection resulted in a significant decrease in the respiratory control index, a significant decrease in ATP level, but no significant change in ADP/O ratio in the liver. Polychlorinated naphthalene was detected by gas chromatography/mass-spectrometry. In the mitochondrial fraction, the shortest retention time component was detected at one hour after the injection. Mitochondria from rats receiving 500 mg/kg of food showed no significant change in the respiratory control index or ADP/O ratio, but a significant decrease in ATP level and an increase in triglyceride levels were observed. Rats fed on the food containing polychlorinated naphthalene at 1000 mg/kg showed significant changes in the respiratory control index and ADP/O ratio of the liver mitochondria, a significant decrease in ATP level and an increase in triglyceride levels.
Acatalasemia and hypocatalasemia mice had decreased levels of mer-cury in the lung and blood and increased levels in the liver following exposure in vivo to metallic mercury vapor (1.4 mg/m3 for 2 hours). The decreased uptake of mercury was roughly proportional to the decrease in catalase activity in these organs. Acatalasemia mice injected with ethyl alcohol showed a decrease in the mercury content of the lung and blood and an increase in the liver content in com-parison with non-treated acatalasemia mice. The inhibitory effect of ethyl alcohol on the uptake of mercury was considered to derive from the peroxidase action of catalase with ethyl alcohol as substrate.
Dealkylation of tetraalkyltin compounds (alkyl: ethyl or butyl) in the intestinal mucosa and in the intestinal contents of the rabbits was investigated in situ and in vitro. Tetraethyl and tetrabutyltin compounds were directly infused into the small intestine isolated in vivo by two forceps after making biliary fistula. Amounts of tetraalkyltin compounds and dealkylated compounds, trialkyltin, in portal vein blood, venous blood, bile, and organs were measured as a function of time after the injection. In the earliest stage, the concentrations of dealkylated compounds in portal vein blood were higher than that in systemic venous blood. This result, together with the finding that no conversion occurs in intestinal contents in vitro, suggests that the conversion of tetraalkyltin compounds into trialkyltin compounds takes place in intestinal mucosa before tetraalkyltin compounds are taken into the liver.