In order to obtain an overall understanding of the toxicity of cadmium (Cd), a single experimental series was designed to investigate the diverse effects of Cd. Four groups of Sprague-Dawley rats, each of which consisted of 14 male and 14 female rats, were administered Cd (CdCl 2) orally at dose levels of 0, 0.1, 1.0, 10.0 mg/kg/day for 6 weeks. After this, the animals were mated for 3 weeks, changing partners every week, for fertility and teratogenicity tests. Cd was given during this mating period. Females were administered Cd during gestation and sacrificed on the 20th day of gestation for fetal examination. After a total of 9 weeks administration, males were subjected to dominant lethal tests by mating 2 females per male per week for 6 weeks. Pregnant females were killed on the 13th day of gestation to test for dominant lethality. This paper reports the results of the general toxicity tests. The main toxic signs, seen only in the 10 mg/kg group, were repression of food intake and body weight gain, depilation, whitening of the incisors, and salivation. Hematological analyses showed that the number of RBC increased while hemoglobin and hematocrit levels decreased, and the number of WBC increased, mainly as a result of neutrophilia. Serum biochemical analyses indicated increased levels of GPT and creatinine, reflecting damage to the liver and kidneys. Increased glucose levels were seen in males. A major change found at the time of autopsy by macroscopic observation of organs was hypertrophy of the jejunum and ileum with a darkish-brown color in nonpregnant females of the 10 mg/kg group. Microscopically, hyperplasia with a high frequency of mitotic figures was seen in the lamina propria mucosae. The weight of the thymus decreased and the weight of the adrenals increased in both males and females. The weight of the ovaries decreased. Major histopathological changes were focal necrosis in the liver and hyperplasia of the adrenal cortices with patchy necrosis in nonpregnant females of the 10.0 mg/kg group. Determination of Cd in the liver and kidneys suggested that excretion of the accumulated Cd was slow. Two aspects of Cd toxicity, i.e., the inhibition of nutrient resorption by unresorbed Cd and the toxicity expressed by resorbed Cd, as well as the causative factors of the adrenal hyperplasia, are discussed.