The influence of androgens on the development and progression of experimentally-induced atherosclerosis has been investigated in nine animal models. Four studies of castrated rabbits with diet-induced atherosclerosis showed either no orbeneficial effects of testosterone on atherosclerotic lesion size in male animals and detrimental effects in female animals (Alexandersen etal. 1999; Bruck etal. 1997; Fogelberg etal. 1990; Larsen etal. 1993). Detrimental effects of testosterone were also seen in male chicks (Toda etal. 1984) and female ovariectomized cynomolgus monkeys (Adams et al. 1995). Interestingly, the sex-specific effects of testosterone in rabbits and monkeys occurred independently of changes in lipid levels (Alexandersen et al. 1999; Bruck et al. 1997) and, surprisingly, despite improved endothelial reactivity (Adams etal. 1995).

Three studies in apoE- or LDL-receptor deficient mice yielded discrepant results (Elhage et al. 1997; Nathan et al. 2001; von Dehn et al. 2001). In the study by Elhage and colleagues (1997), castration at the age of four weeks had no effect on atherosclerosis of either male or female mice. In both sexes, application of subcutaneous testosterone pellets for eight weeks significantly decreased serum levels of cholesterol and inhibited the development of fatty streak lesions in the sinus aortae by about 30%. In the study by von Dehn et al. (2001), suppression of testosterone by 100 |xg of the GnRH antagonist Cetrorelix every 48 hours led to a decrease in atherosclerosis in both the sinus aortae and the ascending aorta despite increases of cholesterol in male and decreases of HDL-C in female mice. Implantation of a silastic implant with 35 mg testosterone led to increases of serum levels of testosterone and cholesterol and atherosclerotic lesion size in male mice. Despite an increase of testosterone levels to 10.1 ng/ml, female mice showed no change in lipids and fewer atherosclerotic lesions. The discrepancy between the two studies may have resulted from the higher dosages of testosterone in the second study. Another study performed in LDL-receptor knock-out mice also found an anti-atherogenic effect of testosterone which was blunted by the parallel use of an aromatase inhibitor. Therefore the anti-atherogenic effect was ascribed to estradiol rather than testosterone (Nathan etal. 2001).

Ta ken together the data of the animal experiments suggest the occurrence of sex-specific effects of exogenous testosterone on atherosclerosis which in male animals may be at least partially mediated by aromatization to estradiol.

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