The findings that normal rat prostates express functional LH/hCG receptors led us to test the hypothesis that benign prostatic hyperplasia (BPH) and prostate carcinomas may also express this receptor gene. The data revealed the presence of LH/hCG receptor transcripts and receptor protein in normal and hyperplastic but not in atrophic glands present in BPH tissue. Smooth muscle and blood vessels in stroma of BPH tissue also contained receptors. Prostate carcinomas contain lower and more heterogeneous receptor levels than BPH tissue. Two human prostate cancer cell lines (LNCaP and DU 145) that were investigated showed the presence of a major 4.5-kilobase transcript and several minor transcripts and also the protein of LH/hCG receptors. However, androgen-sensitive LNCaP cells contained more receptors than androgen-insensitive DU 145 cells. In summary, we demonstrate for the first time that BPH and prostate cancer tissues and cell lines express LH/hCG receptor gene. These findings suggest that higher LH levels in aged men may play a role in BPH and/or prostate carcinomas.

In this study on copper deficiency, the rat crewmaster microcirculation was used as a model for endogenous histamine release and platelet thrombi formation. Male Sprague-Dawley rats were fed either a copper-supplemented diet (CuS, 5 ppm) or a copper-deficient diet (CuD, 0 ppm) for 5 wk before experimentation. The crewmasters of anesthetized rats were spread in a Krebs-filed tissue bath. In venules of CuS animals, photoactivation of intravascular fluorescein isothiocyanate tagged to bovine serum albumin caused significant platelet aggregation and reduction of red blood cell column diameter (RBCCD) by 40 min and stasis of flow by 60 min. In CuD animals there was only minor platelet aggregation and no reduction in RBCCD. Platelet aggregometry studies did not demonstrate reduced platelet aggregation in the CuD group, suggesting that copper deficiency alters the endothelium to inhibit adhesion. Compound 48/80 (1.0 and 10.0 microgram/ml) induced macromolecular leakage in both CuS and CuD groups, with the response in the CuD animals being significantly greater. The results demonstrate that copper deficiency results in alterations of the regulatory mechanisms governing inflammation and thrombosis.

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Summary The effect of dietary copper deficiency on tumour growth, neovascularisation and microvascular integrity was studied in the rat cremaster muscle. Male, weanling Sprague-Dawley rats were fed purified diets which were copper deficient (<0.5 ig g-' of diet) or copper adequate (5 tg g-' of diet). Seven Angiogenesis occurs physiologically in wound healing and in the endometrium. It also occurs in a variety of pathological disorders including diabetes, rheumatoid arthritis, and psoriasis. In addition, there is now considerable experimental evidence that tumour growth and metastasis are also dependent on angiogenesis (Folkman, 1990).A number of factors may modulate the development of new blood vessels in response to angiogenic stimuli (Folkman & Klagsbrun, 1987). In particular, copper deficiency was shown to inhibit angiogenesis in the rabbit cornea induced by prostaglandin E and BALB/C fibroblasts (Ziche et al., 1982). More recently, Brem and co-workers found that a copper deficient diet combined with the copper chelating agent penicillamine inhibited growth of VX2 carcinoma in the brain. Tumours in the rabbit brain remained in an avascular state and failed to develop beyond small nodules. Similar results were observed in the growth and development of rat 9L gliosarcoma (Brem et al., 1990a and b).The only report of the effect of copper deficiency in tumours outside the brain was recently presented (Brem et al., 1990a). In contrast to the brain, where copper deficiency and penicillamine inhibited angiogenesis and tumour growth, there was no inhibition when the same tumour was implanted in the thigh muscle of the same animals. Furthermore, there is limited reported data on the effects of dietary copper deficiency alone (without penicillamine) on tumour angiogenesis (Brem et al., 1990a).In the current study, the effect of diet-induced copper deficiency alone on neovascularisation, microvessel integrity, and growth of an experimental sarcoma was studied in striated muscle. The tumour was implanted into the rat cremaster muscle and the microcirculation was observed in vivo by television microscopy and structurally by light and electron microscopy. Materials and methods Thirty

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