We calculated the intake of each chemical species of dietary arsenic by typical Japanese, and determined urinary and blood levels of each chemical species of arsenic. The mean total arsenic intake by 35 volunteers was 195 f 235 (15.8-1039) pg As day-', composed of 76% trimethylated arsenic (TMA), 17.3% inorganic arsenic (Asi), 5.8% dimethylated arsenic (DMA), and 0.8% monomethylated arsenic (MA): the intake of TMA was the largest of all the measured species. Intake of Asi characteristically and invariably occurred in each meal. Of the intake of Asi, 45-75% was methylated in v i m to form MA and DMA, and excreted in these forms into urine. The mean measured urinary total arsenic level in 56 healthy volunteers was 129 k 92.0 pg As dm-3, composed of 64.6% TMA, 26.7% DMA, 6.7% Asi and 2.2% MA. The mean blood total arsenic level in the 56 volunteers was 0.73 f 0 . 5 7 pg dl-I, composed of 73% TMA, 14% DMA and 9.6% Asi. The urinary TMA levels proved to be significantly correlated with the whole-blood TMA levels (r=0.376; P < 0.01).

In an attempt to establish a method for biological monitoring of inorganic arsenic exposure, the chemical species of arsenic were measured in the urine and hair of gallium arsenide (GaAs) plant and copper smelter workers. Determination of urinary inorganic arsenic concentration proved sensitive enough to monitor the low-level inorganic arsenic exposure of the GaAs plant workers. The urinary inorganic arsenic concentration in the copper smelter workers was far higher than that of a control group and was associated with high urinary concentrations of the inorganic arsenic metabolites, methylarsonic acid (MAA) and dimethylarsinic acid (DMAA). The results established a method for exposure level-dependent biological monitoring of inorganic arsenic exposure. Low-level exposures could be monitored only by determining urinary inorganic arsenic concentration. High-level exposures clearly produced an increased urinary inorganic arsenic concentration, with an increased sum of urinary concentrations of inorganic arsenic and its metabolites (inorganic arsenic + MAA + DMAA). The determination of urinary arsenobetaine proved to determine specifically the seafood-derived arsenic, allowing this arsenic to be distinguished clearly from the arsenic from occupational exposure. Monitoring arsenic exposure by determining the arsenic in the hair appeared to be of value only when used for environmental monitoring of arsenic contamination rather than for biological monitoring.

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We studied the role of S-adenosylmethionine (SAM) as a methyl group donor in the methylation of inorganic arsenic in mammalians. The SAM and S-adenosylhomocysteine (SAH) levels in the livers of untreated hamsters were 74.3± 8.2 and 40.0±6.4 nmol/g, respectively. The SAM level was 63.9±6.5 nmol/g following oral administration of 1.5mg/kg of arsenic trioxide, which was 14% lower than the control level (t-test, p <0.05). This fall of the SAM level in the liver presumably derived from the SAM having acted as a methyl group donor.Oral administration of 1.5 mg/kg of arsenic trioxide once only to hamsters pretreated intraperitoneally with 2.0mg/kg of SAM once only gave the following arsenic levels in the liver and urine. The dimethylated arsenic (DMA) levels in the livers of hamsters treated with SAM plus arsenic trioxide were significantly high, that is, 2 times as high as the control value at 6 hours, and 1.5 times as high as the control value at 24 hours after the administration of arsenic trioxide. The urinary DMA excretion rate in the hamsters treated with SAM plus arsenic trioxide during the first 24 hours after the administration was significantly higher, that is, higher by 36%, than the control value. The urinary DMA excretion rate following pretreatment with SAM was not dose-dependent. Pretreatment with methionine failed to exert any significant acceleratory effect on the methylation of arsenic trioxide.The decreasing pattern of the SAM level in the liver following administration of arsenic trioxide and the DMA behavior in the liver and urine following administration of SAM and arsenic trioxide revealed that SAM accelerated the methylation of inorganic arsenic. In other words, it appeared that SAM could be a very potent methyl group donor to inorganic arsenic.