Since the introduction of 75Se selenomethionine as an agent for pancreatic scanning (1), numerous protocols designed to increase pancreatic uptake of this amino acid analogue have been proposed (1–4). For the most part, these methods have not been substantiated by animal investigation, and, where they have been tested experimentally, no significant increase in pancreatic radioactivity has been found (5). During the past year we have been engaged in determining the effects of numerous hormonal, pharmacologic, and biologic influences on pancreatic amino acid accumulation. Of the agents so far studied, only ethionine has been found to significantly increase pancreatic concentration of 75Se selenomethionine. Ethionine, the ethyl analogue of methionine, has been used, in doses of 1 g/kg body weight, to produce experimental pancreatitis and other cytopathogenic effects in animals (6, 7). When given in smaller daily doses over a period of months, it is carcinogenic (8). We have found in rats that when 1 mg/kg body weight (i.e., one one-thousandth the dose used to produce pancreatitis) of ethionine is given intraperitoneally and 75Se selenomethionine is administered subcutaneously thirty minutes later, a 63 per cent increase in pancreatic radioactivity (over control values) is produced. No significant increase in radioactivity of other organs results. The mechanism of ethionine's effect on accumulation of radioactivity in pancreas appears to reside in suppression of acinar cell enzyme release rather than in increased amino acid uptake or protein synthesis per se (7, 9, 10). It has been conclusively shown that when unlabeled methionine is given simultaneously with ethionine, all adverse cytopathological and physiological effects are prevented (6, 8, 9). We are currently investigating in animals: (a) whether the small dose of ethionine capable of increasing pancreatic amino acid concentration also produces adverse cytopathogenic and physiologic effects and (b) whether administration of unlabeled methionine thirty minutes after 75Se selenomethionine (and thus sixty minutes after ethionine) will prevent the adverse cytopathogenic and physiologic effects of ethionine. We have determined that administration of methionine in such a fashion does not affect the increased pancreatic accumulation of radioactivity. If any adverse effects of the single small dose of ethionine required to augment pancreatic amino acid accumulation can be prevented by subsequent administration of methionine, it should be possible to employ ethionine as an adjunct to clinical pancreatic photoscanning. Since, in practice, the value of pancreatic scanning is limited by relatively unfavorable statistics (i.e., low count rate and poor target: nontarget ratio), a 63 per cent increase in pancreatic radioactivity would represent a considerable advantage. Such an increase might be expected to transform a maximum count rate of, for example, 2500 c.p.m. to 4075 c.p.m.