[Corticotropic and gonadotropic responses to a neurotropic aggression in whole or neonatally castrated male rats. Effect of adrenalectomy].
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Biomedical subjects
Publications and source records attributed to G Lescoat.
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Disappearance of plasma corticosterone after psychic aggression in the prepubertal Rat (25 days) is carried out in a similar manner in the two sexes. At this age, neonatal gonadectomy declined the rate of disappearance. In the adult Rat (60 days) disappearance of plasma corticosterone proceeds more rapidly in females than in males; neonatal gonadectomy abolishes this sex difference. It appears that ovariectomy, contrarily to orchidectomy, decreases the rate of disappearance. Moreover, our results put forward an increased sensitivity of the feedback mechanism corticosterone ACTH during growth.
Evolution during growth of plasma level gonadotropins, was studied in the normal or castrated rat at birth. In the control animals, the plasma level of gonadotropins increased from the 25th day to the 40th day, then declined to the 90th day. Neonatal castration induced a new phenomenon: the increase of plasma gonadotropins in the normal rat corresponded with a decrease in the castrated animals and inversely. Testis hormones affected gonadotropin function; however, an autonomous maturation of this function, independent of gonadal secretions, appeared to exist.
Evolution during growth of plasma level gonadotropins, was studied in the normal rat or castrated at birth. 1. In the control animals, plasma level gonadotropins decreased from the 15th to the 25th day then increased progressively to adult age. 2. Neonatal castration induced a new phenomenon: from the 25th to the 45th day, the increase of plasma gonadotropins in the normal rat corresponded with a decrease in the castrated animals; from the 45th day to the 90th day, plasma gonadotropins increased in the castrated and did not change significantly in the normal animals. 3. Ovary hormones affected gonadotropin function; however, as autonomous maturation of this function, independant of gonadal secretions, appeared to exist.
Plasma LH, FSH and corticosterone were determined between the 15th and 90th day of life, in normal male Rat. Plasma gonadotropins and corticosterone at basal conditions or after psychic aggression increased from the 15th to the 40th or 45th day of life; then all hormones decreased to adult age. The development of plasma gonadotropins and corticosterone are carried out in a parallel manner during the period studied. It was thought that perhaps the elevation of gonadotropins secretion might have stimulated the adrenals.
In the Rat, the estrous cycle induces a rhythm of plasmatic corticosterone level : the fluctuations of basal or stress corticosteronemy are significantly superior during the periods of high estradiol secretion, proestrus and estrus, that during metaestrus and diestrus. Ovariectomy, performed at 60 days of age, is without effect on resting corticosteronemy, but reduces significantly the response to stress. Weaning unaffects the basal level of plasmatic corticosterone which remains comparable to diestrus level ; however, stress response decreased during lactation returns to normal level at the end of the first ovarian cycle (diestrus).
Evolution, during growth, of basal plasma concentration of corticosterone and the adrenocortical response to psychic aggression was studied in animals of both sexes, normal or gonadectomized on the day of birth. 1. In the control animals : (a) The fluctuations of the basal plasma concentration of corticosterone took a similar course in the male and female; no significant difference was observed between males and females except on the 55th day. (b) The intensity of the response to aggression took the same course in all the test animals between the 15th and 60th day with an increase between the 15th and 45th day and a decrease between the 45th and 60th day. 2. In the animals whose gonads were removed at birth, the basal plasma concentration of corticosterone and the response to psychic aggression developed in a similar manner in the two sexes, during the period studied. 3. These results suggest the existence of an autonomous maturation of the adrenocortical function which is independent of genetic sex and gonadal secretions. These latter, however, play a determinant role in the amplitude of the response which is increased by estrogens and decreased by androgens. The existence of a mechanism whose maturation is accomplished, in part, independently of the gonadal secretions and is responsible for the response to aggression is discussed.
1. The plasma corticosterone levels were measured in nursing female rats which had been removed from their pups for 12 hrs, at 9 a. m. every day till weaning (day 22). The mean value found in this condition (14.6 +/- 2.7 mug/100 ml) does not differ significantly from that found for the cyclic female (13.7 +/- 4.2 mug/100 ml). 2. Suckling for a period of either 3 or 30 min increases the content of plasma corticosterone to the same value ; this value is maximal (+ 22.8 mug/100 ml) 30 min after suckling has started. 3. When mothers have been anaesthetized by a pentobarbital injection 40 min before suckling, plasma corticosterone increase, measured in the same conditions, is lower (+ 12.3 mug/100 ml). 4. The response to psychic (+ 25.5 mug/100 ml) or systemic (+ 46.6 mug/100 ml) stresses in mothers which have been removed from pups for 12 hr is impaired with respect to cyclic females (+ 62.7 mug/100 ml and + 83.8 mug/100 ml respectively). 5. Psychic stress applied immediately after suckling does not increase the plasma corticosterone level ; systemic stress does so slightly (+ 25 mug/100 ml). 6. In lactating rats the response to stress of the hypothalamo-pituitary-adrenal axis seems to be the same as that of intact or castrated males or ovariectomized females ; but differs from the response of cyclic females or of pregnant females when their basal corticosterone level is low.
The rates of pituitary and adrenals growth, in male and female Rats, are reversed at puberty. It seems that the stress induced plasma corticosterone increase is inhibited by testis before puberty and stimulated by ovarian after puberty.
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Ethanol-induced lipid peroxidation was studied in primary rat hepatocyte cultures supplemented with ethanol at the concentration of 50 mM. Lipid peroxidation was assessed by two indices: (1) conjugated dienes by second-derivative UV spectroscopy in lipid extract of hepatocytes (intracellular content), and (2) free malondialdehyde (MDA) by HPLC-UV detection and quantitation for the incubation medium (extracellular content). In cultures supplemented with ethanol, free MDA increased significantly in culture media, whereas no elevation of conjugated diene level was observed in the corresponding hepatocytes. The cellular pool of low-mol-wt (LMW) iron was also evaluated in the hepatocytes using an electron spin resonance procedure. An early increase of intracellular LMW iron (< or = 1 hr) was observed in ethanol-supplemented cultures; it was inhibited by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, whereas alpha-tocopherol, which prevented lipid peroxidation, did not inhibit the increase of LMW iron. Therefore, the LMW iron elevation was the result of ethanol metabolism and was not secondarily induced by lipid hydroperoxides. Thus, ethanol caused lipid peroxidation in rat hepatocytes as shown by the increase of free MDA, although no conjugated diene elevation was detected. During ethanol metabolism, an increase in cellular LMW iron was observed that could enhance conjugated diene degradation.
Hereditary Hemochromatosis is an autosomal recessive disease, characterized by chronic iron overload. It is mainly due to mutations of the HFE-1 gene. In the large majority of patients, the substitution of tyrosine for cysteine at amino acid 282 (C282Y) is found at the homozygous state. Since the HFE-1 hemochromatosis identification, several other entities of iron overload have been individualized. In the present article, the frequency, penetrance and pathophysiology of HFE-1 hemochromatosis as well as various clinical presentations resulting from different mutations affecting different proteins involved in iron metabolism are described.
The known relationship between ethanol and the two main proteins of iron metabolism, transferrin and ferritin, are reviewed. Transferrin synthesis decreases in alcoholic cirrhosis, and increases in alcoholic fatty liver. In the latter case, its turnover is accelerated. Serum desialylated transferrin increases in chronic alcoholism and could be the best marker of heavy drinking. The increased uptake of desialylated transferrin by the liver could explain the development of hepatic siderosis in some alcoholics. Serum ferritin increases in chronic alcoholism, much more because of liver damage than in relation to iron stores. It is clear in this review that few experimental studies have been interested in the investigation of these relationships.
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