Effects of Prenatal Exposure to Alcohol on the Release of Adenocorticotropic Hormone, Corticosterone, and Proinflammatory Cytokines

Kim, C. Kwon; Turnbull, Andrew V.; Lee, Soon Y.; Rivier, Catherine

doi:10.1111/j.1530-0277.1999.tb04023.x

Cited by 38 publications

(17 citation statements)

References 61 publications

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“…ACTH and corticosterone secretion showed a peak response at 60 min during endotoxemia ( fig. 1b), followed by a decline, which corresponds to previous findings [46,48]. In the turpentine model, plasma ACTH and corticosterone levels of control animals showed the expected rise during the dark period, while turpentine caused a delayed (14 h) increase in ACTH and corticosterone concentrations that corresponds to the initiation of the IL-6 response [36] (fig.…”

Section: Acth and Corticosteronesupporting

confidence: 59%

“…Serum levels of TNF-· were measured with an ELISA assay specific for rat (R & D Systems, Quantikine M, Minneapolis, Minn., USA) that we previously validated in our laboratory [46]. Serum levels of IL-6 were measured either by bioassay (comparison of the proliferation of the 7TD1 cell line with the interim international recombinant human IL-6 standard (88/154) [24,36,47]) or with a commercially available ELISA purchased from Endogen (Pierce Endogen, Rockford, Ill., USA) [46,48]. While the units reported by these two methods are different, we have previously provided evidence [48] that the relative changes between treatment groups were comparable.…”

Section: Testosterone Lh Acth Corticosterone Tnf-· and Il-6mentioning

confidence: 99%

“…Serum levels of IL-6 were measured either by bioassay (comparison of the proliferation of the 7TD1 cell line with the interim international recombinant human IL-6 standard (88/154) [24,36,47]) or with a commercially available ELISA purchased from Endogen (Pierce Endogen, Rockford, Ill., USA) [46,48]. While the units reported by these two methods are different, we have previously provided evidence [48] that the relative changes between treatment groups were comparable. An important consideration in our choice of the method is that while the bioassay is sometimes considered biologically more relevant, it is very time-consuming and cumbersome.…”

Section: Testosterone Lh Acth Corticosterone Tnf-· and Il-6mentioning

confidence: 99%

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Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Rivier

2002

Neuroimmunomodulation

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Objective: We investigated the ability of foot shocks, endotoxemia and turpentine-induced tissue injury, to interfere with luteinizing hormone (LH) and testosterone (T) secretion, and the putative role of β-adrenergic, opiate- and corticotropin-releasing factor (CRF) receptors in these responses. Methods: Adult male rats were exposed to mild intermittent foot shocks for 1 h, administered endotoxin [lipopolysaccharide (LPS)] intravenously (i.v., 5 µg/kg), or injected with turpentine intradermally (i.m., 400 µl/kg), prior to injection with human chorionic gonadotropin (hCG, 1 U/kg i.v.). In some cases, antagonists to CRF, adrenergic or opiate receptors, or their vehicle were administered prior to the stressors. Levels of LH, T, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), adrenocorticotropin (ACTH) and/or corticosterone were measured in serial blood samples. Results: All three challenges significantly lowered basal LH and T levels and blunted the T response to hCG, though the magnitude of this inhibition was significantly (p < 0.01) smaller in shocked rats (42%), compared to animals injected with LPS (92%) or turpentine (78%). Shocks, LPS and turpentine all significantly stimulated ACTH and corticosterone release, and the magnitude and time course of these responses were also stressor specific. While turpentine only increased circulating IL-6 concentrations, shocks and LPS both significantly increased circulating TNF-α and IL-6 levels, but the effect of shocks was markedly smaller. Pretreatment with propranolol did not restore T responses, while naloxone produced small and inconsistent effects. However, the CRF antagonist Astressin B, which significantly prevented stressor-induced increase in circulating levels of ACTH and corticosterone, partially reversed the inhibitory effect of LPS on hCG-induced T release. Conclusion: (1) Both neurogenic and systemic stressors lower basal plasma LH and T levels and blunt the T response to hCG. (2) LPS, whose ability to release ACTH and corticosterone was similar to that of shocks, but caused increases in circulating TNF-α and IL-6 levels that were significantly larger than those due to the other stressors, was the most potent inhibitor of the T response to hCG. (3) Neither β-adrenergic nor opiate receptors play a major role in the ability of the stressors we used to inhibit T release.

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Section: Acth and Corticosteronesupporting

confidence: 59%

Section: Testosterone Lh Acth Corticosterone Tnf-· and Il-6mentioning

confidence: 99%

Section: Testosterone Lh Acth Corticosterone Tnf-· and Il-6mentioning

confidence: 99%

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Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Rivier

2002

Neuroimmunomodulation

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“…An alternative explanation may, however, involve the influence of the hypothalamic-pituitary-adrenal (HPA) axis. Although the basal levels of corticosterone (16) or ACTH (18) do not appear to be affected by PE exposure, recent evidence demonstrates an augmented response of the HPA axis (11,12,18) to stressors. It is well established that increased corticosterone, or cortisol, can interfere with the stimulated release of AVP (25).…”

Section: Discussionmentioning

confidence: 99%

Prenatal exposure to ethanol causes partial diabetes insipidus in adult rats

Knee¹,

Sato²,

Uyehara³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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ethanol in adult rats and humans leads to reduced AVP-producing neurons, and prenatal ethanol (PE) exposure has been reported to cause changes in the morphology of AVP-producing cells in the suprachiasmatic nucleus of young rats. The present studies further characterize the effects of PE exposure on AVP in the young adult rat, its hypothalamic synthesis, pituitary storage, and osmotically stimulated release. Pregnant rats were fed a liquid diet with 35% of the calories from ethanol or a control liquid diet for days 7-22 of pregnancy. Water consumption and urine excretion rate were measured in the offspring at 60 -68 days of age. Subsequently, the offspring were infused with 5% NaCl at 0.05 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 with plasma samples taken before and at three 40-min intervals during infusion for measurement of AVP and osmolality. Urine output and water intake were ϳ20% greater in PEexposed rats than in rats with no PE exposure, and female rats had a greater water intake than males. The relationship between plasma osmolality and AVP in PE-exposed rats was parallel to, but shifted to the right of, the control rats, indicating an increase in osmotic threshold for AVP release. Pituitary AVP was reduced by 13% and hypothalamic AVP mRNA content was reduced by 35% in PEexposed rats. Our data suggest that PE exposure can cause a permanent condition of a mild partial central diabetes insipidus. fetal alcohol syndrome; vasopressin; plasma osmolality; thirst; vasopressin messenger ribonucleic acid; neurohypophysis CHRONIC CONSUMPTION of alcohol has been shown to significantly reduce the number of AVP-producing neurons in the rat supraoptic nucleus (19). More recently, chronic alcoholism in humans has also been shown to reduce AVP-producing neurons in a dose-related and time-dependent manner (13). Furthermore, AVP synthesis is reduced, as evidenced by reduced AVP mRNA in the hypothalamus of rats chronically administered alcohol, and there is a reduced AVP mRNA response to an osmotic stimulus in similarly treated rats (28). Correspondingly, chronic exposure to alcohol in humans has been reported to reduce plasma levels of AVP (7, 14) and cerebrospinal fluid levels of AVP (23). Thus the AVP system would appear to be impaired by chronic alcohol exposure in adult rats and humans.Previous work has also demonstrated that brain weight is reduced in adult rats that were prenatally exposed to ethanol during the second half of pregnancy (29), and other studies have demonstrated a dose dependence of alcohol-induced brain damage and that some brain structures are more sensitive to the damage than others (21). More specifically, Rojas-Castaneda et al. (26) have reported evidence of morphological changes in the AVP-producing cells of the suprachiasmatic nucleus of 15-dayold rats that were prenatally exposed to ethanol. However, the number of AVP-producing cells was not observed to be significantly reduced in similar studies by the same group (27).Last, there is evidence that AVP systems are nearly fully developed during gestation. AVP has bee...

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“…Interleukin (IL) 6 and tumor necrosis factor (TNF)-␣ were measured as described previously. 20 Statistical Analyses and Reagents. In vitro experiments were performed in triplicate, each repeated at least 3 times.…”

Section: Construction Of Replication-defective Recombinant Adenovirusmentioning

confidence: 99%

Adenovirus-mediated overexpression of follistatin enlarges intact liver of adult rats

Takabe

2003

Hepatology

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Under normal physiologic conditions, liver size is under strict regulatory control. Activin, a member of the transforming growth factor ␤ (TGF-␤) superfamily, is expressed in the intact adult liver and is an inhibitor of hepatocyte growth. However, the exact role played by endogenous activin in maintaining the size of a normal adult liver has yet to be completely examined in vivo. Here, we report the development of an adenoviral vector (AdexCAFS288) that expressed human follistatin-288, which binds to activin and neutralizes its biologic activities. AdexCAGFP, a control virus, expressed green fluorescent protein. AdexCAFS288 effectively expressed follistatin-288, as measured both in HepG2 cell lysate and conditioned medium and blocked activin signaling and its biologic functions in vitro. Intraperitoneal injection of AdexCAFS288 in vivo resulted in significant liver growth (146% of control) in intact liver of adult male rats 12 days following treatment without significant dysfunctions. The increase in liver size was attributed to increased hepatocyte proliferation, as monitored by the mitotic index. Furthermore, there was a significant correlation between serum follistatin levels and liver weight. In conclusion, our results suggest that activin plays a critical role in maintaining optimal liver size and implicates the endogenous activin system as a therapeutic target in the treatment of liver disease. (HEPATOLOGY 2003;38:1107-1115 T he liver has an optimal functional volume that is regulated in relation to body size. 1 When part of the liver is surgically removed, the remaining liver rapidly responds to this alteration by growing back to its original size. 2 Interestingly, the opposite is also true. A transplanted liver that is larger than the optimal size for a particular recipient undergoes apoptosis of hepatocytes and decreases in size until optimal liver volume is reached. 3 These observations suggest that the liver possesses the ability to maintain its optimal functional volume regardless of whether initial liver volume was smaller or larger than standard liver volume. Numerous studies have elucidated mechanisms that initiate and promote liver growth, but few have focused on factors that inhibit liver growth, or decrease liver mass. 4 Activin, a member of the transforming growth factor ␤ (TGF-␤) family of growth and differentiation factors, was first purified as a factor that stimulates follicle stimulating hormone (FSH) release from the pituitary gland. 5 Further work has revealed that activin is widely expressed during development and throughout life and acts as a multipotential growth and differentiation factor in many systems. The administration of exogenous activin inhibited epidermal growth factor-induced growth of primary cultured hepatocytes. 6,7 Previously, we have demonstrated that activin and its signaling partners were expressed in hepatocytes, and endogenous activin negatively regulated hepatocyte proliferation using antisense oligonucleotides directed against activin in vitro. 8 Furthermore, t...

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Effects of Prenatal Exposure to Alcohol on the Release of Adenocorticotropic Hormone, Corticosterone, and Proinflammatory Cytokines

Cited by 38 publications

References 61 publications

Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Prenatal exposure to ethanol causes partial diabetes insipidus in adult rats

Adenovirus-mediated overexpression of follistatin enlarges intact liver of adult rats

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