Effects of vitamin D on insulin secretion and glucose transporter GLUT2 under static magnetic field in rat.

The present study investigated the effects of vitamin D supplementation on insulin secretion and glucose transporter following static magnetic field (SMF) exposure in rat. Wistar male rats were divided into the following groups: control, SMF-exposed rat (128 mT; 1 h/day for 5 days), vitamin D-treated rats (1600 IU/100 g, received by gavage for five consecutive days), and co-exposed rats (the last day and after exposure rats received a single dose of vitamin D per os). Our results showed that exposure to SMF induced an increase in plasma glucose level and a decrease in plasma insulin concentration. Moreover, ß cell insulin content and islet area were lower in SMF-exposed group compared to control. Likewise, we reported the absence of GLUT2 expression in extracellular membrane of pancreatic islet in SMF-exposed group. Interestingly, supplementation with single dose of vitamin D per os corrected insulinemia and glycemia disturbances caused by SMF. By contrast, the same treatment failed to correct pancreatic area. This study provides evidence that vitamin D supplementation has curative effect on pancreas insulin content and on GLUT2 disruption caused by SMF exposure.

Effects of zinc oxide nanoparticles and/or zinc chloride on biochemical parameters and mineral levels in rat liver and kidney.

The aim of this study was to assess the potential subacute toxicity of zinc oxide (ZnO) nanoparticles (NPs) in Wistar rats in comparison with reference toxicant, zinc chloride (ZnCl2), of a non-nanoparticulate form. We therefore studied the relationships between zinc (Zn) accumulation, liver and kidney trace element levels, and plasmatic biochemical parameters. Rats in all groups were treated by intraperitoneal injection of ZnO NPs and/or ZnCl2 solution (25 mg/kg) every other day for 10 days. The contents of trace element in the liver and kidney were slightly modulated after ZnO NPs and/or ZnCl2 solution exposure. The same treatment increased the aspartate aminotransferase activity and uric acid concentration. However, ZnO NPs or ZnCl2 solution decreased the creatinine levels, whereas the combined intake of ZnO NPs and ZnCl2 decreased the glucose concentration. Interestingly, the analysis of the lyophilized powder of liver using the x-ray diffractometer showed the degradation of ZnO NPs in ZnO-treated group, instead there is a lack of NPs ZnO biosynthesis from the ZnCl2 solution injected in rats. These investigations suggest that combined injection of ZnO NPs and ZnCl2 solution has a possible toxic effect in rats. This effect could be related to Zn(2+) ion release and accumulation of this element in organs. Our findings provide crucial information that ZnO appeared to be absorbed in the organs in an ionic form rather than in a particulate form.

Oxidative stress and prevention of the adaptive response to chronic iron overload in the brain of young adult rats exposed to a 150 kilohertz electromagnetic field.

Iron surcharge may induce an oxidative stress-based decline in several neurological functions. In addition, electromagnetic fields (EMF) of frequencies up to about 100 kHz, emitted by electric/electronic devices, have been suggested to enhance free radical production through an iron dependent pathway. The purpose of this study was therefore to determine a possible relationship between iron status, exposure to EMF, and brain oxidative stress in young adult rats. Samples were micro-dissected from prefrontal cortex, hippocampus, striatum, and cerebellum after chronic saline or iron overload (IO) as well as after chronic sham exposure or exposure to a 150 kHz EMF or after combining EMF exposure with IO. The brain samples were used to monitor oxidative stress-induced lipid peroxidation and activity of the antioxidant enzymes superoxide dismutase and catalase. While IO did not induce any oxidative stress in young adult rats, it stimulated antioxidant defenses in the cerebellum and prefrontal cortex in particular. On the contrary, EMF exposure stimulated lipid peroxidation mainly in the cerebellum, without affecting antioxidant defenses. When EMF was coapplied with IO, lipid peroxidation was further increased as compared to EMF alone while the increase in antioxidant defenses triggered by the sole IO was abolished. These data suggest that EMF exposure may be harmful in young adults by impairing the antioxidant defenses directed at preventing iron-induced oxidative stress.

Changes in antioxidant status and biochemical parameters after orally cadmium administration in females rats.

The research was conducted to investigate the toxic effects of cadmium chloride (CdCl2), administered during gestation period on female Wistar rats. Pregnant rats received CdCl2 (20 mg/l, orally) from Day 6 to Day 19 of pregnancy. Results showed that Cd treatment induced a decrease in body weight gain. The relative liver weight increased significantly, with a marked decrease of glycogen and total lipids content. The administration of Cd induced hepatotoxicity as indicated by elevations in plasma alanine aminotransferase (ALT), aspartate aminotransferase and lactate dehydrogenase (LDH) activities (p < 0.05). Treatment with CdCl2 caused a significant (p < 0.05) increase in glucose. A significant increase was observed in the level of MDA and 8-oxodGuo tissues in the cadmium-exposed group compared to the control group (p < 0.05). Results showed that cadmium given to dams led to an oxidative stress and DNA damage in tissues of pregnant rats.

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.

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.

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.

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.

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.

[Implication of type II glucocorticoid receptors in aldosterone induced apoptosis of rat thymocytes]. / Implication des récepteurs glucocorticoïdes de type II dans l'action apoptotique de l'aldostérone sur les thymocytes de rat.

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.

[A physico-chemical analysis of glucocorticoid receptors in corticosensitive and corticoresistant thymocytes: decrease in nuclear transfer]. / Analyse physico-chimique des récepteurs glucocorticoïdes des thymocytes cortico-résistants et cortico-sensibles: diminution du transfert nucléaire.

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.

[Possible implication of TRH and dopamine in postnatal lactotropic hypoactivity in rats]. / Implication possible de la TRH et de la dopamine dans l'hypoactivité lactotrope post-natale chez le rat.

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.

[Postnatal lactotropic hypoactivity in rats: possible implication of VIP, endogenous opioids, dopamine and glucocorticoids]. / Hypoactivité lactotrope post-natale chez le rat: implication possible du VIP, des opioïdes endogènes, de la dopamine, et des glucocorticoïdes.

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.

Involution of rat thymus: characterization of cytoplasmic glucocorticoid receptors, evidence of glucocorticoid resistant dexamethasone receptor-positive cells.

In rats, thymic relative weight increased after birth reaching maximum values between days 15-30 and then decreased markedly in a similar way in both sexes, while the organ's absolute weight continued to increase until days 80-90 and declined slowly with apparent sex differences from day 30 onward. Scatchard analysis revealed that the [3H] dexamethasone (Dexa) receptor sites concentration showed a pattern comparable to that found in relative thymic weight, with no change in the apparent KD. The reduction of lymphocytes mitotic activity resulting in reduction of immature thymocytes production must be accompanied by a fall of the number of glycocorticoid receptors in ageing thymuses. Despite the profound decrease in the glucocorticoid receptor sites levels, the thymus sensitivity to Dexa remained unchanged during development. Indeed, in prepuberal and adult rats, the steroid administration was followed 4 days after by a transient thymic weight loss of about 70-80% which was mainly linked to the reduction in the cortical area. In contrast, the density of [3H] Dexa binding sites was reduced unexpectedly by 25% only after steroid treatment. These findings provided evidence that Dexa receptor-positive population cells in thymus was formed in a large part by relatively glucocorticoid resistant cells.

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)

[Effects of different acute and chronic stresses on general growth and adrenal cortex activity in rats]. / Incidence de différentes agressions aiguës et chroniques sur la croissance générale et l'activité corticosurrénalienne chez le rat.

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.

[Effects of exhaust gas on adrenal cortex activity, general growth and variation of intermediate metabolism in the male rate during a period of growth]. / Incidence du gaz d'échappement sur l'activité corticosurrénalienne, la croissance générale et la variation de certains métabolismes intermédiaires chez le rat mâle en période de croissance.

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.

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.