This work was undertaken to find if a study of oxidation-reduction potentials, pH and oxygen tension would yield information concerning physiological changes induced in lactating mammary glands of rats and rabbits by hormones and other substances. Breathing oxygen at atmospheric pressure caused a rapid rise in oxygen tension in lactating mammary gland, and a small, slower rise of oxidation-reduction potential. Breathing nitrogen had the opposite effect. Oxytocin caused a rapid temporary fall of oxidation-reduction potential, synchronous with milk ejection. With adrenaline the response was more rapid and the oxygen tension fell to zero, to recover within 2 min. Vasopressin produced a slower fall and recovery. Insulin (35
μ
g/kg) caused a preliminary rise of oxidation-reduction potential, followed by a fall lasting 1 h. The fall could be largely abolished by glucose. The synthetic oestrogen doisynolic acid caused a triphasic response in the oxidation-reduction potentials and increased oxygen tension in the gland. It reduced, but did not abolish, the changes due to insulin. Desoxycorticosterone glucoside caused a slow rise of oxidation-reduction potential, but did not alter the response to insulin. Intermedin caused a small rise of oxidation-reduction potential. The effects produced by commercial ACTH may have been due to the oxytocin and intermedin present. Growth hormone induced a small diphasic change in the oxidation-reduction potentials. The radiosensitizers tetrasodium 2-methyl-1:4-naphthohydroquinone diphosphate and tetrasodium trimethyl-hydroquinone diphosphate produced marked falls of oxidation-reduction potential even with small doses, without change of oxygen tension. Intravenous potassium ferricyanide appeared to liberate oxygen from haemoglobin
in vivo
. The pH of mammary gland became slightly more acid after breathing oxygen, and also in the preliminary response to insulin, glucose, doisynolic acid and desoxycorticosterone glucoside; and after oxytocin, vasopressin and growth hormone.