AIM:To better darify the main target organs of dimethylarsinicacid toxicity and the role of metallothionein (MTs) inmodifying dimethylarsinic acid (DMAA) toxicity.METHODS:MT-Ⅰ/Ⅱ null (MT~(-/-)) mice and the correspondingwild-type mice (MT~(+/+)),six in each group,were exposed toDMAA (0-750 mg/kg body weight) by a single oral injection.Twenty four hours later,the lungs,livers and kidneys werecollected and undergone pathological analysis,induction ofapoptotic cells as determined by TUNEL and MT concentrationwas detected by radio-immunoassay.RESULTS:Remarkable pathological lesions were observedat the doses ranging from 350 to 750 mg/kg body weight inthe lungs,livers and kidneys and MT~(+/+) mice exhibited arelatively slight destruction when compared with that in dosematched MT~(-/-) mice.The number of apoptotic cells wasincreased in a dose dependent manner in the lungs and liversin both types of mice.DMAA produced more necrotic cellsrather than apoptotic cells at the highest dose of 750 mg/kg,however,no significant increase was observed in the kidney.Hepatic MT level in MT~(+/+) mice was significantly increased byDMAA in a dose-dependent manner and there was nodetectable amount of hepatic MT in untreated MT~(-/-) mice.CONCLUSION:DMAA treatment can lead to the inductionof apoptosis and pathological damage in both types of mice.MT exhibits a protective effect against DMAA toxicity. AIM: To better darify the main target organs of dimethylarsinicacid toxicity and the role of metallothionein (MTs) in modifying dimethylarsinic acid (DMAA) toxicity.METHODS: MT-I / II null (MT ~ (- / - type mice (MT ~ (+ / +)), six in each group, were exposed to DMAA (0-750 mg / kg body weight) by a single oral injection. Twenty four hours later, the lungs, livers and kidneys were collected and undergone pathological analysis, induction ofapoptotic cells as determined by TUNEL and MT concentrationwas detected by radio-immunoassay.RESULTS: Remarkable pathological lesions were observedat the doses ranging from 350 to 750 mg / kg body weight inthe lungs, livers and kidneys and MT ~ (+ / - +) mice showed arelatively slight destruction when compared with that in dosematched MT ~ (- / -) mice.The number of apoptotic cells was established in a dose dependent manner in the lungs and liversin both types of mice. DMAA produced more necrotic cellsrather than apoptotic cells at the highest dose of 7 50 mg / kg, however, no significant increase was observed in the kidney. Hepatatic MT level in MT ~ (+ / +) mice was significantly increased by DMAA in a dose- dependent manner and there was node can not dose amount of hepatic MT in untreated MT ~ (- / -) mice.CONCLUSION: DMAA treatment can lead to the induction of apoptosis and pathological damage in both types of mice. MT exhibited a protective effect against DMAA toxicity.