PHARMACOLOGY OF THALLIUM 
7 
to disturbances of the calcium metabolism {21^ 33^ 35, 37). Be- 
cause of these disturbances, conditions resembling rickets are pro- 
duced, with a progressive failure of the body tissues to store calcium. 
Histological examinations of the skeletal bones showed definite evi- 
dence of rickets {36, 37) . 
In a further series of papers {13, H, 16, 16, 17, 18, 19, 20, 22, 26, 
26, 27, 28, 29, 31, 32, 31^, 38, 39, iO, Jfl, ^3, JfS, 78), Buschke and co- 
workers showed that thallium poisoning was developed through its 
actions upon various endocrine glands. This accounts for the failure 
of tadpoles to grow in very dilute solutions of thallium salts. The 
action is specifically exerted upon the ovaries or testicles, which may 
completely atrophy ; in a number of rats, complete loss of the testicles 
was produced; in others no spermatozoa could be found. The 
epinephrine content of the suprarenal glands was greatly decreased. 
Involvements of the thyroid gland were also found. Evidence 
regarding the effect upon the pituitary gland was not so definite, 
although some involvement seemed demonstrable. Cataracts were 
produced in rats {78) and also proliferation of the mucosa of the 
cardiac end of the stomach. 
Dal Collo (4<^, 49) confirmed the endocrine action of thallium 
upon rabbits. Six rabbits weighing 2,500 to 2,800 grams were given 
10 milligrams of thallium acetate intravenously the first day, and 
the daily dose increased 10 milligrams until death supervened on 
the fifth or sixth day. Guinea pigs were given 1 milligram subcu- 
taneously the first day, and the dose increased by 0.5 milligram a day 
until death, on the thirteenth to sixteenth day. Rats were fed 1 
milligram daily in their food. All animals showed parenchymatous 
and vascular nephritis, with characteristic epithelial lesions, and 
diffuse changes in the convoluted tubules. 
Transitory hyperglycemia, followed by constant hypoglycemia; 
sexual changes, but no congenital eye lesions or lesions of the bones 
or parathyroid gland ; leucocytosis ; and erythropenia were observed 
in rats following the administration of thallium salts. No relation or 
interdependence could be established between alopecia, hypertrophic 
processes, bone lesions, and the appearence of cataracts by Mamoli 
{103, 101^) in 1926. 
Olivier {113) observed that long feeding of small doses of thallium 
to rats caused inflammatory proliferations of the mucosa of the 
esophagus and cardiac end of the stomach. Ehrhardt {69) went a 
step further in the study of the action of thallium upon the newborn ; 
a female rat was fed large doses of thallium for four days, after 
which she died. The nursing young were at once transferred to a 
normal lactating rat and fed her milk, but all showed the typical 
effects of thallium poisoning. This clearly demonstrates the harm- 
ful action of thallium upon the young, whether the transference 
occurs in utero or in the milk. 
Buschke and Peiser {38) experimented with an organic thallium 
compound, thallium dimethyl bromide. The lethal dose to mice was 
found to be 5 to 6 milligrams per mouse, or 10 times the lethal dose 
of thallium acetate. Similar symptoms were produced. The 
hydrogen-ion concentration of thallium solution influenced the rate 
of amphibian metamorphosis (7). The pathological changes pro- 
duced in various animals by thallium have been investigated by 
