Species differences in the response to dietary MoO4(2)- as a metabolic antagonist of Cu are considered briefly. Suggestions that (i) the potency of MoO4(2)- as a Cu antagonist is enhanced by normally innocuous dietary concentrations of S20 and (ii) that MoS4(2)- may be a more effective antagonist than either MoO4(2)- or S2- were investigated in a series of studies with rats. Diets including MoS4(2)- but not of MoO4(2)- or S2- alone promoted a decline in hepatic Cu and ceruloplasmin activity and induced clinical signs of Cu deficiency. Evidence of concurrent anomalies in the partition of Cu between tissues and in the distribution of Cu between proteins of plasma and kidney cytosol suggested that such effects were partly attributable to the development of systemic defects in Cu metabolism. The relationship of such findings to the suggested involvement of MoS4(2)- or its derivatives in the etiology of Mo-induced Cu deficiency in ruminant animals is considered.