Thymic neoplasm. A surgical enigma.
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17-Ketosteroids↗
Biomedical subjects
R R Watson
Publications and source records attributed to R R Watson.
Solid benign tumors of the esophagus.
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Esophageal Neoplasms↗
Pulmonary rheumatoid nodule with cavitation and chronic lipid effusion.
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Humans↗
Functional and numerical alterations induced by ethanol in the cellular immune system.
Ethanol was found to alter functioning and numbers of lymphoid cells of the cellular immune system in humans and rats. In in-vitro studies on human lymphocytes, a higher than 0.1% concentration of ethanol and acetaldehyde and acetic acid, the metabolites of ethanol, caused a decrease in the formation of E-rosettes. Methanol and propanol also resulted in a decrease in E-rosette formation. The natural killer (NK) cells varied in their ability to lyse tumor cells. In vitro, the NK-cell activity declined at higher than 0.2% concentration of ethanol. The NK activity in cells isolated from spleen and thymus of rats fed 1 g/dl or 7 g/dl ethanol did not differ significantly from the controls. Sprague Dawley rats fed 1 g/dl or 7 g/dl ethanol for 12 weeks had a significantly smaller thymus compared to the controls. Alveolar macrophages isolated from the rats exhibited impaired phagocytic activity. In agreement with other investigators, ethanol was found to result in a loss of T-cell population in the spleens of rats fed ethanol for 13 months. On the other hand, the T-helper cells and the proportion of T-helper to T-suppressor cells were found to increase in the splenocytes from these rats. This latter occurrence, apparently, is to compensate for the general loss of T-cell population observed in the body that occurs with ethanol ingestion. It is hypothesized that immunosuppression and the transient imbalances in the components of the cellular immunity induced by ethanol lead to an increased risk of pathogenesis associated with alcohol consumption.
Animals↗
Vitamin E reduction of lipid peroxidation products in rats fed cod liver oil and ethanol.
The purpose of this study was to investigate the effects of vitamin E supplementation on ethanol- and cod liver oil-induced lipid peroxidation. Adult male rats received diets containing ethanol, cod liver oil and supplemented with vitamin E for 28 days. Following treatment, hepatic conjugated dienes, lipid fluorescence, and exhalation of ethane were measured as indices of lipid peroxidation. Ethane expiration over a 3-hour period was reduced by 96% in rats fed ethanol supplemented with vitamin E. Exhalation of ethane was increased by CLO feeding but was reduced 89% in the CLO-fed rats supplemented with vitamin E. In addition, ethane production was elevated in rats fed ethanol plus CLO compared to rats fed diets containing CLO supplemented with vitamin E. Supplementation of the CLO diet with vitamin E also significantly decreased hepatic conjugated fatty acid dienes levels. Levels of hepatic conjugated fatty acid dienes from rats fed ethanol plus vitamin E were reduced 91% compared to rats fed ethanol diets. Additionally, hepatic lipid fluorescence expressed as per mg of hepatic phospholipid basis was also significantly increased in rat groups fed vitamin E, ethanol, and cod liver oil diets. Where vitamin E was added to these same diets a significant decrease of hepatic lipid peroxidation products occurred. The observed reduction in lipid peroxidation by vitamin E may be useful to retard lipid peroxides derived materials involved in the development of alcoholic liver diseases.
Animals↗
Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue.
Lipid peroxidation products and the fatty acid composition of phospholipids were studied in the hearts of rats chronically consuming ethanol supplemented with large amounts of vitamin E. Ethanol representing 36% of the total calories was ingested for 7 weeks in a modified Lieber-DeCarli liquid diet that contained vitamin E at 30 IU/L in the control or 172 IU/L in the supplemental dietary group. Ethanol and/or vitamin E did not change the absolute content (micrograms per mg of phospholipids) of the main fatty acids (C18:0, C18:2, and C20:4) of heart phospholipids but increased the amount of the minor C20-C22 fatty acids. Cardiac phospholipid levels increased in rats chronically consuming excess vitamin E and/or alcohol. Chronic ethanol consumption caused elevations of the relative content (percent of total fatty acids) of tri-, tetra-, and hexaenoic acids and peroxidizability index (PI) of the cardiac phospholipids. Supplementation with vitamin E blocked this ethanol-induced shift in the fatty acid profile toward unsaturation and decreased the PI. Ethanol enhanced accumulation of vitamin E in heart tissue by 30% irrespective of the vitamin E content in the diet. Enrichment of the diet with vitamin E coincided with the low levels of fluorescent products in heart lipids. A positive correlation (r = 0.36; p = 2%) was found between vitamin E and diene conjugates in the heart cells. Thus, vitamin E has a stabilizing effect on heart phospholipids by preventing changes in their fatty acid composition and peroxidative deterioration.
Alcoholism↗
Ethanol and cytokine secretion.
Cytokines are regulatory polypeptides secreted during the generation of an immune or inflammatory response by lymphocytes, cells of the monocyte/macrophage series, and a variety of other cell types. Alterations in the production, site of action, or metabolism of cytokines by exogenous factors, such as ethanol (EtOH), may have deleterious effects on the immune system as a whole. EtOH has been implicated in the onset of a variety of immune defects in vivo including effects on the production of cytokines critically involved in inflammatory responses (tumor necrosis factor, interleukin 1 and interleukin 6). In this review, we examine current knowledge regarding the effects of EtOH on the release of cytokines in humans and in animal models, in vitro and in vivo, which may help to elucidate the adverse actions of EtOH on mammalian immune systems.
Animals↗
Ethanol enhances immunosuppression induced by cocaine.
Use of cocaine concurrently with alcohol is prevalent among cocaine addicts. Cocaine has been shown to inhibit phytohemagglutinin- and ConA-induced proliferation of T-lymphocytes, NK cell cytotoxicity, and phagocytic activity of peritoneal macrophages. In some studies no effects of cocaine on the immune response have been observed, although on the contrary, others show it increased the NK cell activity and serum antibody response to T-dependent antigen. Effects of cocaine on the immune system may be mediated by its neurostimulatory action on the hypothalamo-pituitary-adrenal axis. ACTH, beta-endorphine, and corticosterone released under the action of cocaine exert various inhibitory effects on the immune function. We studied the immunotoxic effect of cocaine, combination of cocaine with ethanol, and cocaethylene, a derivative formed from cocaine and ethanol in the body, on the mitogen-stimulated production of cytokines by splenocytes. C57BL mice were injected twice daily with 20 mg/kg cocaine or equivalent dose of cocaethylene and received a liquid Lieber-DeCarli diet containing ethanol (26% of total calories) or isocaloric amount of maltose-dextrin. After 3 weeks of treatment, cocaine and cocaethylene caused a significant decrease of the spleen weight and total number of splenocytes. In splenocytes isolated from the cocaine- or cocaethylene-treated mice, mitogen-stimulated production of gamma-interferon, tumor necrosis factor, and interleukin-2 was suppressed, in all cases more severely when cocaethylene was used. Thus, formation of cocaethylene during simultaneous consumption of cocaine and ethanol may enhance the immunotoxicity of cocaine.
Animals↗
Alcohol stimulation of lipid peroxidation and esophageal tumor growth in mice immunocompromised by retrovirus infection.
Tumor appearance can be accelerated in the immunodeficient and immunosuppressed animal. The role of lipid peroxidation and immune dysfunction induced by retrovirus and ethanol treatments on cancer promotion were investigated. Following the initiation of esophageal cancer by methylbenzylnitrosamine, ethanol consumption and retrovirus infection individually and concomitantly increased growth of esophageal tumors. Dietary supplementation with vitamin E reduced the size and frequency of the developed tumors. Tumor growth modifications in the vitamin E supplemented animals may be due to changes in T-cell numbers and functions stimulated by vitamin E. In addition, increased production of free radicals following ethanol treatment and retrovirus infection, and the suppression of these formations lipid peroxide by vitamin E is accompanied by lower incidence and size of tumors. Thus, the mechanisms of tumor enhancement observed in immunocompromised animals may include a combination of immunomodulation and modification of oxidant production by ethanol consumption and retrovirus infection.
Acquired Immunodeficiency Syndrome↗
Ethanol-induced changes in the intestinal mucosa-associated immune system of young and mature mice.
Alcoholics have frequent bronchial and intestinal bacterial-associated infections compromising the mucosal-associated lymphoid tissues. Alcoholics also suffer undernutrition due to changes in their lifestyles. Thus, we studied the intestinal mucosa-associated lymphoid tissues using two types of diets in young and mature mice. The objective was to elucidate if ethanol consumption alters the T and B cell populations in the intestine, and if the alteration could be associated with the age and/or the nutritional status of the host. There was an increase in the number of CD8+ cells per field in the intestinal lamina propria (ILP) of young mice consuming ethanol, with no change in CD4+ and IgA+ cells in the ILP and CD4+ and CD8+ cells in the intestinal intraepithelium (IE). There was also an increase in the number of CD4+ and CD8+ cells in the ILP of well-nourished mature mice consuming ethanol, and an increase in the number of CD4+ cells in the ILP of undernourished mice. An increase in the number of CD8+ cells in the IE was also detected in the well-nourished group consuming ethanol. Therefore, we conclude that ethanol administration alters the intestinal mucosa-associated lymphoid tissue.
Aging↗
Is alcohol consumption a cofactor in the development of acquired immunodeficiency syndrome?
Excessive alcohol (EtOH) consumption and acquired immunodeficiency syndrome (AIDS) are two major public health problems in the United States. Overwhelming evidence is showing that heavy EtOH ingestion broadly suppresses the various arms of immune response, seriously impairing the body's normal host defense to invading microbes and tumorigenesis. The onset of clinical symptoms of AIDS (low CD4+ T cells count, opportunistic infections, and tumors) is quite variable among HIV+ individuals with a mean incubation time 3-10 years following seroconversion. Because of the deleterious effects of chronic EtOH consumption on cytokine release, immune response, host defense, nutritional status, and oxidative stress, it has been believed to be a possible cofactor that could enhance the host's susceptibility to infections, and subsequently increase the rate of AIDS development. The purpose of this review is to present evidence indicating clinical disorders during EtOH ingestion in murine AIDS. These EtOH-induced abnormalities may promote a more rapid development of AIDS in HIV-infected individuals.
Acquired Immunodeficiency Syndrome↗
Chronic ethanol consumption prior to retrovirus infection alters cytokine production by thymocytes during murine AIDS.
Chronic ethanol (EtOH) consumption may be a cofactor in the development of acquired immune deficiency syndrome (AIDS). As the thymus is an unique site for T cell maturation, we investigated whether thymocytes from EtOH consuming mice were more predisposed to aberrant cytokine production due to retrovirus infection. Adult female C57BL/6 mice were fed 4.5% (v/v) in liquid diet or control liquid diet without EtOH for 10 weeks. All diets contained nutrients at only the recommended daily intake level for mice. Then all mice were infected LP-BM5 retrovirus and were fed control liquid diets without EtOH. The body and thymus weights were not affected by EtOH consumption. However, thymocyte number and proliferation, which had been reduced during murine AIDS, were significantly further reduced by EtOH use. The production of IL-2 and IL-6 by thymocytes, which was lessened during retrovirus infection, were significantly further suppressed by dietary EtOH at 6 weeks postinfection, whereas levels of IL-4 and IFN-gamma by thymocytes, which were elevated during retrovirus infection, were significantly and slightly further increased by EtOH-treated mice prior to retrovirus infection, respectively. These data suggest that dietary EtOH consumption can modulate cytokine production by thymocytes, adversely affecting T cell differentiation, especially during retrovirus infection. These results provide additional evidence that EtOH consumption should be a cofactor during development of AIDS via producing altered cytokine production and then disrupting T cell differentiation.
Alcoholism↗
The effect of alcohol consumption on nutritional status during murine AIDS.
As alcohol (ETOH) abusers and AIDS patients have nutritional disorders, the influence of chronic ETOH consumption (5% v/v for 10 weeks) on levels of immunomodulatory nutrients (vitamins A and E, Zn, and Cu) in the serum, liver, small intestine, spleen, and thymus was determined during murine AIDS. The hepatic levels of vitamins A and E and Zn in both normal and LP-BM5 retrovirus-infected female C56BL/6 mice fed ETOH were significantly reduced compared to controls, whereas the level of Cu in the liver was not affected. Intestinal levels of vitamin A and Cu were not affected by ETOH, whereas vitamin E and Zn were significantly reduced in both normal mice and those with AIDS fed ETOH. The splenic levels of vitamin A and Zn in the normal mice were significantly reduced by ETOH compared to controls, but vitamin E and Cu were not. All splenic levels of nutrients measured were reduced in ETOH-fed mice with AIDS. The levels of vitamins A and E, Zn, and Cu in the thymus in murine AIDS were also significantly affected by ETOH consumption. The serum levels of vitamins A and E in both normal mice and murine AIDS were significantly decreased by dietary ETOH. These data produced evidence that chronic ETOH can directly aggravate undernutrition initiated by retrovirus infection. Such ETOH-induced malnutrition in AIDS may be a cofactor, accelerating development of AIDS via immunosuppression secondary to nutritional deficiencies.
Animals↗
Ethanol, immune responses, and murine AIDS: the role of vitamin E as an immunostimulant and antioxidant.
Excessive alcohol consumption is a major health problem in the United States. Prolonged consumption of alcohol results in alterations of immune responses, ultimately manifested by increasing susceptibility to infectious agents. Such changes can be due to the direct effects of alcohol or its metabolites on immune cells, as well as to nutritional deficiency, oxidative stress, and neutrophil dysfunctions. This ETOH-induced immunosuppression could be a potential cofactor in the progression to AIDS. As vitamin E supplementation has been associated with enhancement of immune response and improvement of host defense, it may provide a useful therapeutic approach for treatment of alcoholics to improve host defense. This article is a review of alcohol-related immunosuppression as a possible cofactor in the development of AIDS, and vitamin E-related immunoenhancing roles in animals and humans, showing why vitamin E supplementation could be used as a useful adjunct agent in alcoholics' treatment. Since there is little information available regarding nutritional therapy with alcohol users, our purpose is to provide evidence from animal models of the potential therapeutic role of vitamin E supplementation in the treatment of alcoholics.
Acquired Immunodeficiency Syndrome↗
Alterations in mouse Peyer's patch lymphocyte phenotype after ethanol consumption.
The objective of this study was to determine if chronic ethanol consumption could modify cell populations in the Peyer's patches (PP), which could favor pathogenic or opportunistic infections in mice, as seen in chronic alcohol addicts. Young C57BL/6 mice receiving the Lieber-DeCarli diet (36% of calories as ethanol) for 5 weeks presented a significant decrease in the total number of cells in the PP. Mature FVB mice receiving the Lieber-DeCarli diet for 19 weeks presented a highly significant decrease in the total number of cells and in the absolute number of T and B cells in the PP. Young C57BL/6 mice receiving the 100% NRC (30% ethanol) or the 60% NRC (30% ethanol) diets for 7 weeks presented alterations in the T and B cell phenotype comparable with the alterations observed in mice receiving the Lieber-DeCarli diet for 19 weeks. As less alcohol for a shorter time caused similar changes to those seen with a highly micronutrient enriched diet with more alcohol for a longer consumption period, micronutrient supplementation may overcome some immune damage found in animal models of alcoholism. Our data indicated that ethanol administration altered the mucosal immune system at the level of the PP, the site for antigen presentation and induction of a mucosal immune response.
Alcoholism↗
Alcohol consumption alters cytokine release during murine AIDS.
Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a human immunodeficiency virus (HIV), representing the end point in a progressive sequence of immunosuppressive changes. HIV, the key causative agent of AIDS, induces immunosuppression that render the body highly susceptible to opportunistic infections and neoplasm. However, the onset of clinical symptoms of AIDS (e.g., low CD4+ T cells count, opportunistic infections, and tumors) is quite variable among HIV+ individuals with a mean incubation times 3-10 years following seroconversion. Because of the deleterious effects of chronic alcohol (EtOH) consumption on cytokine release, immune response, host defense, nutritional status, and oxidative stress, it has been believed to be a possible cofactor that could enhance the host's susceptibility to HIV infection, and subsequently accelerate the development of AIDS. The purpose of this review is to present evidence of EtOH-induced cytokine dysregulation during murine AIDS. Our results done in murine AIDS indicate the EtOH consumption may accelerate the development of AIDS by disrupting cytokine production. These EtOH-induced abnormalities in cytokine release may promote a more rapid development of AIDS as a cofactor, which exacerbates the immune dysfunctions initiated by retrovirus infection.
Animals↗
Validation of conductance catheter system for quantification of murine pressure-volume loops.
The purpose of this study was to define the validation methods and outcomes of a conductance catheter system specifically for in vivo murine cardiac hemodynamic analysis. To express the relationship between conductance and blood volumes, we used an in vitro model to derive a volume-conductance line. The volume-conductance line was used to compute raw volume from the modified conductance signals. The parallel volume was calibrated with hypertonic (15%) saline injected from extrajugular vein. The ventricular volume was computed by raw volume minus parallel volume. The accuracy of conductance volumetric measurements was validated with a static in situ infusion of calibrated volumes of whole blood injected into arrested left ventricles. In vivo dynamic measurements were performed with 24 C57B1/6 mice, 6 months old; for comparison of established values. The in situ model showed that after calibration, the experimental coefficient, alpha, was equal to 1 and the measured volume by conductance catheter was equal to the true volume of the left ventricle (y = 0.982x + 0.513, p < .0001). For the in vivo models, the end-diastolic volumes and the stroke volumes and cardiac output determined with the conductance catheter system were 17.3 +/- 1.0 microL, 10.6 +/- 0.9 microL, and 6.0 +/- 0.5 mL/min, respectively. We validated the relationship between measured volume by conductance catheter and the true volume and demonstrated the accuracy of the volume-conductance line for conversion of conductance to volume.
Animals↗
Enzyme activities support the use of liver lipid-derived ketone bodies as aerobic fuels in muscle tissues of active sharks.
Few data exist to test the hypothesis that elasmobranchs utilize ketone bodies rather than fatty acids for aerobic metabolism in muscle, especially in continuously swimming, pelagic sharks, which are expected to be more reliant on lipid fuel stores during periods between feeding bouts and due to their high aerobic metabolic rates. Therefore, to provide support for this hypothesis, biochemical indices of lipid metabolism were measured in the slow-twitch, oxidative (red) myotomal muscle, heart, and liver of several active shark species, including the endothermic shortfin mako, Isurus oxyrinchus. Tissues were assayed spectrophotometrically for indicator enzymes of fatty acid oxidation (3-hydroxy-o-acyl-CoA dehydrogenase), ketone-body catabolism (3-oxoacid-CoA transferase), and ketogenesis (hydroxy-methylglutaryl-CoA synthase). Red muscle and heart had high capacities for ketone utilization, low capacities for fatty acid oxidation, and undetectable levels of ketogenic enzymes. Liver demonstrated undetectable activities of ketone catabolic enzymes but high capacities for fatty acid oxidation and ketogenesis. Serum concentrations of the ketone beta-hydroxybutyrate varied interspecifically (means of 0.128-0.978 micromol mL(-1)) but were higher than levels previously reported for teleosts. These results are consistent with the hypothesis that aerobic metabolism in muscle tissue of active sharks utilizes ketone bodies, and not fatty acids, derived from liver lipid stores.
Aerobiosis↗