Steroid-induced cataract: other than in the whole animal system, in the lens culture system, androgens, estrogens and progestins as well as glucocorticoids produce a loss of transparency of the lens.
OBJECTIVE
To investigate the mechanism of glucocorticoid-induced cataract formation, the lenses of chick embryos were cultured with androgen, estrogen and mineralocorticoid as well as glucocorticoids. The incidence of loss of transparency induced by these steroids in the culture system and the whole body system was compared.


METHODS
In the culture system, clear lenses obtained from 16-day-old chick embryos were treated with various concentrations of steroid hormones for 48 h at 37 degrees C in a humidified atmosphere containing 5% CO2. In the whole body system, these steroids dissolved in 5% acetone in water were administered to 15-day-old embryos and the lenses were isolated and visually classified on day 17.


RESULTS
When 0.25 mumol of steroids were administered to 15-day-old chick embryos, only biologically active glucocorticoids such as hydrocortisone and prednisolone could cause cataract. Dexamethasone is approximately 25-fold stronger than hydrocortisone and prednisolone. Methyltestosterone as an androgen, estradiol and ethinylestradiol as estrogen, progesterone and 19-nor-ethisterone as progestin did not induce cataract formation. In the whole body system, the cataracts were caused with a dependence on the biological activity of glucocorticoids. However, other than in the whole body system, when the isolated chick lenses were cultured in the dishes, they could become opaque in the presence of testosterone, estradiol and aldosterone as well as dexamethasone and hydrocortisone at a similar dose (over 3 x 10(-5) M).


CONCLUSIONS
These results demonstrate that the loss of transparency of cultured lens can be induced independently from biological activities of steroids. Glucocorticoids have various physiological and pharmacological activities in the living system. We assume that the steroid-induced cataract is one of the adverse effects caused by synergic biological activities of glucocorticoids.
Kosano
Hiroshi
H
Faculty of Pharmaceutical Sciences, Teikyo University, Sagami-ko, Tsukui-gun, Kanagawa, Japan.
Nishigori
Hideo
H
D000728:Androgens / Q000494:pharmacology*; D000818:Animals; D002386:Cataract / Q000139:chemically induced* / Q000473:pathology; D002642:Chick Embryo; D004967:Estrogens / Q000494:pharmacology*; D005938:Glucocorticoids / Q000494:pharmacology*; D007908:Lens, Crystalline / Q000187:drug effects* / Q000196:embryology; D009924:Organ Culture Techniques; D011372:Progestins / Q000494:pharmacology*
D000728:Androgens; D004967:Estrogens; D005938:Glucocorticoids; D011372:Progestins