Variations of Acute Iodide Toxicity Among Inbred Strains of Mice

Abstract

Although there is scant information concerning the lethal effects of acute iodide intoxication, most evidence indicates individual variability. In man, individual idiosyncrasies predispose certain persons to iodism, a relatively mild reaction to low levels of administered iodides(l). Occasionally, death occurs in newborn infants whose mothers receive repeated doses of iodides during gestation. The lethal effects in these cases may result from the development of huge goiters which interfere with respiration(2). Such occurrences are infrequent, suggesting that individual sensitivity is involved in these deaths. In rats and dogs, massive doses of iodide cause pulmonary edema, often followed by death; Trotter suggests that production of pulmonary edema by iodide is related to its anti-thyroid activity (3).

That some aspects of iodine metabolism are under genetic control is indicated by variations of thyroid activity among several lines of inbred mice and their Flhybrids (4). Evidence presented here shows that acute iodide intoxication is also controlled by genetic factors.

Materials and methods. Mice of various strains (Table I), 30-90 days of age, were injected intraperitoneally with 10% aqueous Nal and observed daily for 14 days. In early experiments, it was noted that all mice killed by the treatment died within 5 days. Thereafter, mice still alive after 14 days were listed as survivors. The LD₅₀ and its 99% confidence interval were calculated using the Spearman-Karber method(5). Approximately equal number of males and females were used in each group. With the exception of the ICR Swiss and CFW stocks, the mouse strains had been inbred for at least 20′ generations. The CFW stock was obtained from Carworth Farms, inbred for 10 generations and maintained subsequently by random breeding. The ICR Swiss mice have been random bred since the stock was established.