PubMed · 4160940
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K Torizuka, T Kono, S Hamada, M Kawase, K Nakaie. 1965. [Hormone-binding proteins].. https://pubmed.ncbi.nlm.nih.gov/4160940/
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It has previously been shown that morphine can increase the frequency of micronucleated splenocytes when administered to mice, but not when cells are exposed to the opiate in vitro. Morphine treatment is also known to increase circulating levels of glucocorticosteroids, which have been reported to produce genetic damage in vivo and in vitro. In order to determine whether adrenal hormones might mediate the genotoxic effects of morphine, adrenalectomized and sham-operated mice were treated with morphine sulfate. In sham-operated animals administration of morphine produced a dose-related increase in the frequency of micronucleated cells, whereas adrenalectomy abolished the effect. When plasma from morphine-treated mice was used to supplement growth medium of untreated splenocytes, the frequency of micronucleated cells increased, an effect partially blocked by the steroid antagonist RU 486. The N-methylmorphine, which does not stimulate the release of corticosterone from adrenal glands, induced micronuclei formation in splenocytes, and administration of metyrapone, an inhibitor of corticosterone biosynthesis, blocked the morphine-induced increase in corticosterone secretion, but had no effect on the frequency of micronuclei formation. These results indicate that basal levels of glucocorticosteroids are required for induction of micronuclei by morphine in murine splenocytes, but activation of the hypothalamo-pituitary-adrenal (HPA) axis by morphine does not contribute to the observed response.
In each of 4 years, 94-116 mature cows had two 6-7-day-old embryos, produced by the in vitro fertilisation of oocytes, inserted non-surgically into one uterine horn of each cow. Starting 5 days before the expected date of calving, the cows were continuously observed and assistance at calving was provided when required. In year 1, perinatal calf survival was similar in twin-calving (TC) and single-calving (SC) cows (98.1 versus 100% for calves born to TC and SC, respectively). There was a higher incidence of assistance at birth for TC (52%) than for SC (21%). In years 2 and 3, the calving of 30 SC and 33 TC was synchronised using an injection of Opticortinol (OP) 6-9 days before the injection of Estrumate and Dexol-5 (E+D). A further 34 SC calved naturally. Synchronised calving reduced the spread of calving from 16-25 to 8-9 days without reducing perinatal calf survival and had no significant effect on the incidence of assistance at birth in SC. The TC in years 2 and 3 had a high incidence of retained placenta at 48 h (70%) and a high incidence of assistance at birth (85%). In year 4, calving was synchronised in 16 SC and 21 TC with E+D and no pre-treatment with OP, while 15 SC were treated with both OP and E+D. There were no effects of the hormone treatment on perinatal calf survival and only small effects on the incidence of assisted births for SC. The incidence of retained placenta at 48 h was lower for SC pre-treated with OP (40%) than for SC (88%) and TC (76%) not pre-treated with OP. Continuous supervision over calving produced perinatal calf survival rates for TC that were similar to SC, despite the higher incidence of assistance of TC at parturition. Hormonal synchronisation of calving can halve the time required for continuous supervision of calving, but the hormone treatments exacerbate the already high incidence of retained placenta in TC.
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