Abstract
cells responded to luteinizing hormone, human chorionic gonadotropin, isoproterenol, and cholera toxin with an increase in progesterone and cyclic AMP responses. Administration of 4-aminopyrazolo(3,4~)p~midine (4-UP) (12.5 mgfkg body weight) for 3 consecutive days reduced the circulating cholesterol level from 47.32 2 1.12 mg/dl to 8.16 & 0.43 mg/dl and plasma progesterone from 280 f 26 ng/ml to 96 k 6 ng/ ml. Cellular sterol ester content was reduced to 25% following 4-APP injection. Injection of drug also produced a small but significant decrease in luteal cell free cholesterol. Treatment of rats with 4-APP also reduced the in vitro basal and hormone-stimulated progesterone production. This treatment showed no effect on luteal cell ‘251-human chorionic gonadotropin binding or gonadotropin and cholera toxin stimulated cyclic AMP synthesis. Exposure of luteal cells isolated from control and 4-APP injected groups to homologous or heterologous lipoproteins (low and high density lipoproteins) produced significant stimulation in steroidogenesis, both under basal conditions and in response to gonadotropins. Similarly, luteal cells isolated from 4APP-injected rats incorporated [3H]cholesterol from [3~~cholesteryl linoleate into progesterone at a much faster rate compared to control cells, and this effect was further enhanced in response to human chorionic gonadotropin. Injection of rats with Triton WR 1339 (1 g/kg body weight) resulted in a 10-fold increase in circulating cholesterol level. This treatment, however, produced a significant decrease in plasma progesterone and cyclic AMP and progesterone responses in isolated cells. The inhibitory effect of Triton injection on steroidogenesis could not be reversed by lipoprotein addition. These studies suggest that rat luteal cells are acutely dependent upon exogenous lipoprotein cholesterol for the maximum expression of steroidogenic response.
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