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Biomedical subjects

M Sakly

Publications and source records attributed to M Sakly.

At least 19 recordsLinked to original sources
PubMed2005

Skeletal muscle HSP72 and norepinephrine response to static magnetic field in rat.

The present work was undertaken in order to investigate the noradrenergic system and skeletal muscle heat shock protein 72 (HSP72) response to static magnetic field (MF) in male rats. At thermoneutrality (25 degrees C), the exposition of rats 1 hour/day for 5 consecutive days to MF of 128 mT (m tesla) induced an increase in norepinephrine content in gastrocnemius muscle (+25%, p < 0.05) but had no effect at 67 mT (+1%, p > 0.05), indicating a stimulatory effect of sub-acute MF exposure on the noradrenergic system activity. Moreover, exposed rats to MF displayed a non-significant increase of HSP72 levels in gastrocnemius muscles (+29%, p > 0.05). The results indicate that noradrenergic systems in rat's gastrocnemius muscles are affected by MF exposure. Interestingly, sub-acute exposure insufficiency increased HSP72 levels in gastrocnemius muscles.

Animals↗
PubMed2003

Electrical conduction through nerve and DNA.

The aim of the present study was to analyse electric resistivity at different ambient temperatures between 300 to 20K in the frog sciatic nerve and salmon sperm DNA. When the electrical contacts were leaned just into the sciatic nerve, an increase of the sciatic nerve resistivity was observed for 240 K < T < 300 K and a rise of electrical conductivity was apparent below 240 K. This dependence is generally associated with a semiconductor behaviour. Once the sciatic nerve temperature was driven below 250K, the resistivity abruptly decreased and then at temperatures lower than 234 K, it remained constant and close to one tenth of its ambient temperature value. By contrast, when the electrical contacts were leaned into Salmon sperm DNA, the resistivity remained constant between 300K to 20K, showing a high electrical stability at low temperature. Thus, we report the existence of a new form of electric conductivity in the sciatic nerve at low ambient temperature, which in turn has many electric similarities with inorganic or organic superconductors, whereas temperature failed to alter DNA electrical properties until 20K.

Animals↗
PubMed2003

Successful pregnancies after using immotile spermatozoa from ejaculate, epididymis and testis.

OBJECTIVE: To assess the efficacy of intracytoplasmic sperm injection (ICSI) in term of pregnancy rate with immotile spermatozoa from ejaculate, epididymis and testis. STUDY DESIGN: A retrospective study was conducted between January 1998 and March 2001. We performed intracytoplasmic sperm injection with immotile spermatozoa, in 160 couples during 172 cycles. RESULTS: The birth rate per cycle was 38.4% in immotile spermatozoa from ejaculate, 35.4% from testis and 38.7% from epididymis. CONCLUSION: This retrospective analysis shows that immotile spermatozoa retrieved from epididymis or testicle gives similar fertilization and pregnancies rates as immotile spermatozoa from ejaculate.

Ejaculation↗
PubMed2001

Reproductive toxicity of DDT in adult male rats.

The reproductive toxicity of DDT was investigated in adult male rats exposed to 50 and 100 mg/kg body weight (b.wt) day(-1) for 10 successive days. Compared with control animals, administration of DDT led to a dose-dependent reduction of testicular weight and the number as well as the percentage of motile spermatozoa in the epididymis. Testicular histological observations revealed also a marked loss of gametes in the lumen of seminiferous tubules. In DDT-treated rats, the seminal vesicles weights dropped significantly, resulting from a decrease of testosterone production by testes, whereas serum LH and FSH increased after pesticide exposure. This increase of gonadotrophin levels may be related to an impairment of the negative feedback exerted by the steroid on the hypothalamic--pituitary axis. It is concluded that DDT induced adverse effects on male rat fertility by acting directly on the testes and altering the neuroendocrine function.

Animals↗
PubMed2000

Acute hepatotoxicity of DDT: effect on glucocorticoid receptors and serum transcortin.

The hepatotoxic effect of 1,1 bis (p-chlorophenyl) 2,2,2 trichloroethane (DDT) treatment for 10 consecutive days has been examined in Wistar rats. DDT exposure increased relative liver weight, dose dependently, with a marked decrease of glycogen content and profound histological changes including cytoplasmic vacuolization, signs of necrosis and nuclear enlargement. The hepatomegaly induced by DDT (50 and 100 mg/kg body weight day-1) appeared not to be accompanied by a significant alteration of the hepatic glucocorticoid receptor concentration and affinity while, serum corticosteroid binding globulin level increased slightly with the lower dose of the pesticide. It is concluded that a short-term exposure to DDT did not lead to a status stress and, therefore, the hepatotoxic effect of organochlorine seemed not to be mediated by endogenous glucocorticoids.

Animals↗
PubMed1997

[Implication of type II glucocorticoid receptors in aldosterone induced apoptosis of rat thymocytes].

The thymolytic action of dexamethasone (DEXA) and aldosterone (ALDO) has been studied in vitro and in vivo. In vitro, in the presence of DEXA, the number of apoptotic cells increased with time. After 6 hours of incubation, 55 and 86% of thymocytes are dead with 10(-7) and 10(-5) M of DEXA, respectively. Whereas, in the presence of equivalent concentrations of ALDO, the rate of mortality of cells was only 30-40%. In vivo study confirmed these results and showed that apoptotic action of ALDO remained less potent than that of DEXA. On the other hand, addition of the potent glucocorticoid antagonist, RU 38486 prevents not only the dexamethasone but also the aldosterone-stimulated cell death. We conclude that the thymolytic action of the endogenous mineralocorticoid hormone is not mediated by its specific receptor but paradoxically by type II glucocorticoid receptor.

Aldosterone↗
PubMed1997

[A physico-chemical analysis of glucocorticoid receptors in corticosensitive and corticoresistant thymocytes: decrease in nuclear transfer].

We have demonstrated in prior work that the density of cytoplasm receptors was comparable in DEXA-resistant and DEXA-sensible thymocyte populations (1). The present study was aimed at examining whether the resistance of thymocytes to the lytic action of glucocorticoids was linked or not to variation in the physico-chemical properties of the receptor itself. Our results show that the cytoplasmic receptors of DEXA-resistant thymocytes were, in terms of specificity, stability and elution profile on DEAE Sephacel columns, similar to those of DEXA-sensible cells. However, under condition of identical concentrations of DNA and receptors, we revealed a decrease in the nuclear transfer of glucocorticoid receptor in the DEXA-resistant thymocytes. This deficiency may account in part for the glucocorticoid resistance of these cells which may be related to intrathymic cell differentiation phenomenon.

Animals↗
PubMed1996

[Possible implication of TRH and dopamine in postnatal lactotropic hypoactivity in rats].

Our results show that pituitary glands of young rats (6 days) incubated in vitro, increase their PRL secretion in presence of TRH, this responses is greater than that in adult glands. Indeed, in presence of TRH 10(-7) M, PRL basal secretion of immature glands passes from 478.70 +/- 67.25 to 952.78 +/- 67.02, versus 5333.29 +/- 75.456 and 6347.15 +/- 75.246 ng/mg protein at mature glands. The same dose of dopamine (DA), weakens the TRH stimulating effect by 60% and 40% respectively by young and adult pituitary glands. These results suggest that lactotroph insensitiveness to TRH injection observed during the first days of postnatal life at the rat, would not be explained by lactotroph failure, but by intervention of central and peripheral multiple modulator factors affecting lactotrophs reactivity, in particular the importance of dopaminergic control.

Animals↗
PubMed1996

[Postnatal lactotropic hypoactivity in rats: possible implication of VIP, endogenous opioids, dopamine and glucocorticoids].

In this study, the possible intervention of VIP (Vasoactive Intestinal Peptide), beta-endorphine, glycocorticoids and dopamine, in postnatal lactotrophs hypoactivity at the rat, was investigated. Our results show that the injection of VIP (40 micrograms/kg), beta-endorphine (125 micrograms/kg) or its antagonist, naloxone (2 mg/kg), does not provide a change in serum PRL before or after ether stress at 6-day-old rats. However, after adrenalectomy, 6 day-old neonates became sensitive to ether stress as do adults, while acute treatment with dexamethasone (2 mg/kg) or dopamine (1 mg/kg), abolished this response completely. Sulpiride injection (1 mg/kg), on the contrary potentialized response. This lactotroph insensitiveness to ether stress, TRH, VIP, and beta-endorphine, during the beginning of postnatal life in the rat, might be explained, partially, by the failure of stimulatory factors "PRF" (Prolactin Releasing Factors), together with strength of inhibitory factors "PIF" (Prolactin Inhibitory Factors), such as dopamine and glycocorticoids.

Animals↗
PubMed1988

Impairment of stress-induced secretion of prolactin during development: effects of adrenalectomy, TRH and sulpiride.

Ontogeny of serum and anterior pituitary gland PRL contents was investigated. Pituitary PRL concentrations were found to be low in fetus by 19th day of gestation and to rise slowly after birth with no sex differences being apparent until day 30. Adult levels were reached in males on day 15, while in females they were reached beyond this stage. Serum PRL levels exhibited a similar developmental pattern. In adult rats ether stress stimulated basal serum PRL significantly, with maximum effect one minute after onset of stress. The same pattern was seen with immature animals of 15-20 and 30 days of age. In contrast, in 2 or 6 day-old neonates, serum PRL concentrations remained unaffected by stress. This lack of responsiveness suggests the existence of a transient impairment of lactotrophs to respond to stressful stimuli during postnatal life. Adrenalectomy increased PRL release in adult and newborn rats from day 15 onward and potentiated the response of lactotrophs. Moreover, after adrenalectomy, 6 day-old rats became sensitive to ether stress, while acute treatment with dexamethasone abolished completely this response. In adult or 15 day-old neonates administration of TRH or sulpiride resulted in a marked increase in serum PRL levels. However, at 6 days TRH did not affect resting serum PRL concentrations significantly, whereas sulpiride remained efficient. Moreover, at this age, dopamine inhibited stress-induced PRL release and reduced the stimulatory effect of sulpiride.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1985

[Effects of different acute and chronic stresses on general growth and adrenal cortex activity in rats].

Stress due to ether, physical strain, and exhaust gas applied to pubescent male rats either acutely or chronically, (15 days or 2 months) always induce a similar increase of plasmatic corticosterone. However, they induce other different changes (food intake, body growth, protein yield, and the relative growth of the liver, the testis and the heart). Thus we define for each type of aggression a non-specific action, characterized by a more or less similar activation of the pituitary-adrenal axis and an other specific action.

Acute Disease↗
PubMed1984

Paradoxical involvement of glucocorticoid receptors in the aldosterone-induced impairment of ACTH secretion from perifused pituitary glands.

The present investigation was aimed at examining whether interaction of aldosterone with specific mineralocorticoid receptors at the level of the pituitary gland may account for the inhibitory effect of that steroid on ACTH secretion. By using pituitaries from neonatal rats, which we show to completely lack specific mineralocorticoid receptors but to contain a functional glucocorticoid receptor system, we demonstrated the persistence of aldosterone-induced inhibition of ACTH release from perifused glands. Conversely, when the glucocorticoid receptors sites were blocked in pituitaries from mature rats by means of a potent antiglucocorticoid (RU 38486), thus leaving unaltered mineralocorticoid binder, aldosterone no longer dampened hormonal output. We conclude that the latter steroid affected corticotropic activity by interacting not with its proper and specific receptor, but rather with the glucocorticoid binding sites.

Adrenocorticotropic Hormone↗
PubMed1984

[Effects of exhaust gas on adrenal cortex activity, general growth and variation of intermediate metabolism in the male rate during a period of growth].

The exhaust gas induces a stressing action, similar to classical type agression: activation of the pituitary adrenal-axis, with increase of relative adrenal weight, and of the rate of corticosterone production. After chronic exposure, deep metabolic changes appear, which reflect an accentuated state of exhaustion of the organism. Moreover perturbation of spermatogenesis with azoospermia is noted. Thus exhaust gas is to be considered as a very potent toxic agent.

Adrenal Cortex↗
PubMed1983

Ontogenetical variations of transcortin modulate glucocorticoid receptor function and corticotropic activity in the pituitary gland.

This study was aimed at investigating the influence of tissue and plasma transcortin on pituitary glucocorticoid receptor function and corticotropic activity during development. "In vivo" nuclear uptake of (3H)corticosterone was found to be increased in pituitary glands from newborn rats which, unlike that of adults, lack transcortin-like material. Immature glands incubated "in vitro" likewise showed enhanced nuclear accumulation of tracer; the magnitude of uptake being inversely related to both tissue and plasma contents of transcortin. Competition studies indicate that pituitary transcortin modulates interaction of corticosterone with receptor binding sites and, hence, may interfere with steroid translocation to the nucleus. Moreover, we found that steroid-induced inhibition of ACTH release was highest in those pituitaries which were deficient in transcortin-like molecules. We conclude that the binder plays a modulating role in pituitary glucocorticoid receptor function.

Adrenocorticotropic Hormone↗
PubMed1982

Physicochemical analysis of glucocorticoid receptor in the immature pituitary gland: evidence for lability and aggregation of the heat-activated form.

The present study was aimed at characterizing the deficiency of the glucocorticoid-receptor system in the immature pituitary gland of neonatal rats. Under conditions of both constant protein and DNA concentrations, [3H]dexamethasone binding to nuclei was significantly lower in the immature, compared with the mature, glands, despite the comparable density of receptor sites. Chromatography on DEAE-Sephacel columns revealed the failure of the neonatal receptor to form stable activated complexes, although the dissociation of tracer from binding sites, as well as the magnitude of receptor activation, remained closely similar to those found for the adult binder. Also, a striking observation was that the immature receptor exhibited the property of forming more than twice as much inactive aggregate as the mature component, when heat-activated in presence of KCl. It thus seems that development of full expression of glucocorticoid-binding activity in the pituitary involves qualitative changes of both the receptor molecules and the cytoplasmic environment, that tend to enhance stability of the activated form of the binder.

Animals↗
PubMed1981

Modulation by transcortin-like binding sites of uptake and distribution of glucocorticoids by dispersed pituitary cells.

The influence of transcortin-like (TL) binding sites on uptake and distribution of glucocorticoids by dispersed pituitary cells was investigated. TL material, which combines corticosterone (CORT), but not dexamethasone (DEX), was previously found to be present on cell membranes and in cytosol of hypophysis. Exposure of cells at 0 degrees brought about striking differences in steroid binding, as labeled CORT was taken up more rapidly and to a significantly greater extent than DEX. This resulted from a higher concentration of binding sites and not from a difference in binding affinity. At 25 and 37 degrees, while the same relationship was apparent during the early events of steroid interaction with the cell, binding of DEX increased gradually with incubation time and finally exceeded that of the natural steroid. Also, time-course studies on nuclear translocation showed a biphasic pattern, which closely paralleled that of whole-cell binding. Interestingly, treatment of rats with transcortin antiserum caused a decrement of pituitary TL sites, as well as of CORT translocation. We conclude that the TL binder, which is probably of plasma origin, may be actively involved in the process of uptake and cellular distribution of corticosteroids in the pituitary gland.

Animals↗