The influence of biosynthetic human growth hormone on biomechanical properties (strain at maximum load, maximum load, relative failure energy, maximum stiffness) and collagen content of intact rat skin was measured after injection of biosynthetic human growth hormone for 90 days at doses of 0.16, 1.10 and 8.33 mg\m=.\kg\m=-\1 \m=.\ day\m=-\1. The mechanical test showed that strain at maximum load, maximum load and relative failure energy increased with increasing doses of biosynthetic hGH. In the group receiving 8.33 mg \ m=. \ kg\m=-\1 \ m=. \ day\m=-\1, skin = Newton. J = joule. Mean values 1 sem. 1 2P< 0.05 compared with placebo. Spearman's for relative failure energy = 0.45 (P< 0.01).Bruvvers, Oxford.

Selenium intake (5.0 ppm) induces growth retardation, accumulation of selenium in somatotrophs, lack of growth hormone response to GHRH and an 80 per cent reduction in serum somatomedin C in infant rats. In addition, it induces a slight reduction in serum albumin and occasionally slight central liver necrosis. In order to determine the role of insufficient growth hormone production, the influence of exogenous growth hormone was studied during selenium intake in groups of rats during 25 to 46 days of age (post-weaning). A dosage of human growth hormone (100 \ g=m\ g twice daily) was chosen, this being sufficient to restore normal growth rate and normal serum somatomedin C in hypophysectomized rats of similar age. The weight gain in selenium-treated (3.3 ppm) rats was 46.0 \m=+-\11.7 g (sd)/21 days, whereas in selenium rats given growth hormone it was 66.6 \m=+-\8.9 g (P = 0.01), which was similar to the gain in control rats 72.3 \m=+-\6.9 g. The latter two were less than the weight gain in control rats given growth hormone: 91.5 \m=+-\11.5 g (P = 0.01 and P < 0.01). Serum somatomedin C in untreated rats was 151 \m=+-\66(SD) \g=m\g/l (25 days) increasing to 532 \m=+-\ 91 \ g=m\ g/ l (34 days) and 482 \ m=+-\64 \g=m\g/l(46 days). It did not increase above these levels in control rats given growth hormone. In selenium-treated rats, no increase occurred during growth hormone administration 138 \m=+-\148 \ g=m\ g/ l (34 days) and 185 \m=+-\84 \g=m\g/l(46 days) (P < 0.001 and P < 0.001 vs untreated controls). Furthermore, there was no reduction in serum protein or albumin and no liver necrosis in these selenium-treated rats. As exogenous administration of growth hormone normalizes weight gain, the results indicate that growth retardation is at least partly due to insufficient growth hormone production. The increased growth rate in seleniumtreated and control rats given growth hormone appears to be independent or circulating somatomedin C. This may be a direct effect of growth hormone or, more likely, may be caused by GH stimulation of peripheral (paracrine) formation of growth factors, possibly somatomedin C.