Abstract
Cadmium nitrate (Cd(NO3)2; CdN) is commonly used in Ni-Cd battery factories. However, there are few reports regarding the kinetics of CdN. This study was designed to investigate the early dynamic state of Cd in the blood, bile, and urine in rats as a model of accidental occupational exposure to CdN. It was also designed to determine the relationship between the kinetics and harmful effects of CdN. To evaluate the kinetics of CdN exposure and metabolism, rats received a single intravenous injection of CdN (2.1, 4.2, or 6.3 mg/kg). Serum Cd concentrations were determined 0, 5, 10, 30, 60, 120, and 300 min after the injection. Calculating the elimination data of Cd from serum required two-compartment modeling. Bile was collected at intervals of 30 min until 300 min. Urine was collected for 300 min. T1/2 β, MRT and AUC0→300 were significantly longer, and the total body clearance, V1 and Vss were significantly lower in the 6.3 mg/kg group than those in the other groups. Total biliary and urinary Cd excretion levels were higher in the 6.3 mg/kg group than those in the other groups. Our previous study indicated that acute exposure to CdN causes severe liver and proximal tubular damage, particularly at a dose of 6.3 mg/kg. Abnormalities in Cd kinetics could result from extensive hepatic dysfunction at a toxic dose. This dysfunction could lead CdN to sensitive cellular targets, such as the kidneys, over long periods of time. Kinetics abnormalities and liver and kidneys dysfunctions may enhance CdN toxicity.
