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Biomedical subjects

R R Watson

Publications and source records attributed to R R Watson.

At least 145 records · Page 8Linked to original sources
PubMed1991

Effects of prolonged ethanol consumption on hepatic lipids and hepatotoxicity in C57BL/6 female mice.

Mice consume high levels of alcohol for a short period of time resulting in increased toxicity and lethality. The effects of lower doses that could be consumed without death for prolonged periods were studied. The effects of moderate doses of ethanol on indices of lipid peroxidation (LP), liver lipid accumulation and hepatotoxicity were studied in C57BL/6 mice. Three groups of mice were fed diets in which ethanol provided 0, 25 or 30% of the total calories for 3, 7, 10 and 13 weeks. Increased hepatic cholesterol, phospholipid and triglycerides, indicative of changes in liver lipid metabolism; and increased levels of hepatic malondialdehyde, conjugated dienes, lipid fluorescence, serum alanine aminotransferase and minimal changes in liver architecture indicative of LP and liver damages, were observed in mice fed the alcoholic diets. Such increases were time and dose dependent. These results suggest that continuous ingestion of lower levels of dietary ethanol in mice produces biochemical and hepatotoxic responses which are indicative of the health risk often associated with high alcohol intake.

Alanine Transaminase↗
PubMed1991

Cocaine and the pregnant woman.

The growing use of cocaine among pregnant women and its effects on the fetus have attracted national attention. Increasing amounts of data are now available showing the specific negative obstetric, perinatal and neonatal complications. This review examines specific aspects of cocaine use during pregnancy, including pharmacology, effects on pregnancy and childbirth, perinatal and neonatal outcome, and detection of drug use.

Cocaine↗
PubMed1991

The potential role of vitamin E in the treatment of immunologic abnormalities during acquired immune deficiency syndrome.

The literature is briefly summarized as to immunologic modifications caused by the human acquired immune deficiency syndrome (AIDS), immunocompetence at various nutritional states of vitamin E, and the immunoenhancing properties of vitamin E. The abnormalities of immune components present in AIDS are similar to those that are stimulated or restored by intake of high doses of vitamin E. Dietary supplementation of vitamin E with an adequate nutrition support or concomitant use of this vitamin with current drug therapies [For example, Zidovudine (AZT)] may increase the therapeutic efficiency of drugs and enhance immune resistance to opportunistic infections associated with AIDS. Supplementation with vitamin E may also decrease the progression of the disease to AIDS. Unlike many pharmacological agents which are toxic at low levels, vitamin E is non-toxic over a wide range of intakes. A moderately high dose may be used to target and stimulate some specific immune cells destroyed by HIV infection. However, further interdisciplinary studies are much needed to relate various levels of intake of this vitamin as a supplement to clinical outcomes during HIV infection and establish the role for this vitamin in human immunity during AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1991

The effect of vitamin E (alpha-tocopherol) supplementation on hepatic levels of vitamin A and E in ethanol and cod liver oil fed rats.

Eight groups of 5 rats were fed 8 differing liquid diets with and without ethanol, cod liver oil and/or increased levels of vitamin E. Hepatic levels of vitamins A and E were determined following the 28-day feeding time. Ethanol consumption decreased the levels of hepatic vitamin E (p less than 0.05), vitamin A (p less than 0.05) and the ratio of vitamin A/E (p less than 0.05). Hepatic levels of vitamins A and E were unaffected in rats fed cod liver oil. Supplementation of the normal dietary level of 30 IU of vitamin E per kg diet, with an additional 142 IU alpha tocopherol/kg diet, restored hepatic concentrations of vitamin E to normal levels in alcohol-fed rats. The hepatic levels of vitamin A in rats fed ethanol diets supplemented with vitamin E were less than that of control rats but were 4.3 times greater than that of rats on ethanol diets unsupplemented with vitamin E. However, the vitamin A and E ratio was equal to normal in this group of rats. The vitamin A/E ratio was reduced in liver of rats fed non-alcoholic diets supplemented with vitamin E due to increased levels of hepatic vitamin E. Additionally, rats fed cod liver oil diets containing ethanol also indicated decreased hepatic vitamin A and E levels. However, these levels were greater than that of rats fed only alcoholic diets suggesting that these vitamins are replaced by the vitamin A and E content in the cod liver oil.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1990

Hair analysis.

Explore the source record for details and available documents.

Animals↗
PubMed1990

Effects of cocaine and morphine on IgG production by human peripheral blood lymphocytes in vitro.

Elevated serum levels of IgG are amongst the immunological abnormalities exhibited by intravenous drug addicts. We therefore addressed the hypothesis that cocaine and morphine (the major metabolite of heroin) exert a direct effect on human B cell function in vitro. Human peripheral blood mononuclear cells from normal individuals were incubated for 7 days with the T cell-dependent B cell activator pokeweed mitogen (PWM) and serial dilutions of either cocaine or morphine. At the end of this time total IgG was measured by use of a sandwich ELISA incorporating a biotin-labelled affinity-purified anti-IgG and streptavidin peroxidase. At concentrations relevant to those found in plasma, morphine and cocaine did not affect PWM-stimulated IgG synthesis in vitro. We suggest that these drugs of abuse do not directly influence human B cells, but in vivo exert immune modulatory effects via indirect mechanisms.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Immunomodulation by cocaine--a neuroendocrine mediated response.

Cocaine acts directly on lymphoid cells and indirectly modulates the immune response by affecting the level of neuroendocrine hormones. In vitro, very high concentrations of cocaine inhibit different immune responses, while plasma levels following cocaine use have no effect. The results of the few published in vivo studies are contradictory, showing stimulatory, suppressive or no effect on lymphoid cells. The indirect effects of cocaine on the immune system could be mediated by ACTH, beta-endorphin and corticosterone. Anorectic effect associated with nutritional deficiencies of drug users could additionally affect the immune response by cocaine.

Animals↗
PubMed1990

In vitro immunotoxicology and immunopharmacology: studies on drugs of abuse.

The application of immunotoxicology to the toxicologic assessment of drugs of abuse is a field of increasing importance. Interest in the effects of drugs of abuse on the immune system has greatly increased as a result of the AIDS epidemic. If drugs of abuse compromise the immune system, their use may well become a predisposing factor in the development or enhancement of AIDS in high-risk groups. Therefore development and validation of newer methods of assessment of immunotoxicology and their adaptation to routine analysis is an absolute necessity. An important feature in toxicology in general, and in immunotoxicology in particular, is the need to develop in vitro assessment systems. Recent research has provided newer models, data on correlations of immune function variables, and a better understanding of the biologic relevance of certain immune function parameters. This paper analyzes these features in relation to the role of drugs of abuse in the modulation and alteration of the immune system and reviews the various in vitro techniques that could be used to evaluate immunotoxicity.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Nutritional effects of marijuana, heroin, cocaine, and nicotine.

Use of addictive drugs, such as cocaine, marijuana, and nicotine, affects food and liquid intake behavior, taste preference, and body weight. Changes in specific nutrient status and metabolism can also develop; heroin addiction can cause hyperkalemia and morphine use can result in calcium inhibition. Nutrition-related physiological aspects, such as impaired gastrin release, hypercholesterolemia, hypothermia, and hyperthermia, are also seen with morphine use. Nutrition-related conditions can affect sensitivity to and dependence on drugs and their effects. Diabetes decreases sensitivity to and dependence on morphine, protein deprivation produces preferential fat utilization with low cocaine use, and vitamin D deficiency decelerates morphine dependency. During use and/or withdrawal from nicotine, heroin, marijuana, and cocaine, major changes in food selection and intake occur, which result in weight gain or loss. Detailed human studies are needed to investigate the effects of drug use on the broad spectrum of nutrients and to determine the role of nutrition during drug withdrawal.

Animals↗
PubMed1989

Enhancement of the expression of activation markers on human peripheral blood mononuclear cells by in vitro culture with retinoids and carotenoids.

Retinoids (retinol, retinal, retinoic acid, retinyl beta-glucuronide, and 13-cis retinoic acid) and carotenoids (beta-carotene and canthaxanthin) were evaluated for their immunomodulatory effects on human peripheral blood T-lymphocyte subpopulations and natural killer (NK) cells. Peripheral blood mononuclear cells (PBMC) from healthy young volunteers were isolated and incubated for 72 hours at various levels of retinoids and carotenoids including a physiological concentration (10(-8) M). Expression of surface antigens for total T cells, T-helper and T-suppressor cells, and activation markers (transferrin receptor, HLA-Dr antigen, and interleukin 2 receptor) were analyzed with an EPICS V flow cytometer. Retinoic acid and 13-cis retinoic acid (13-cRA) produced significant increases in the percentage of cells with markers for total T-helper cells, with a minimal effect on percentage of lymphocytes with markers for NK cells. However, beta-carotene (BC), canthaxanthin (CTX), and retinyl beta-glucuronide (RBG) dramatically increased the percentage of PBMC with markers for NK cells and produced a smaller increase in lymphocytes with surface antigens identifying them as T-helper cells. Furthermore, retinol and retinal did not show significant change either in the percentage of lymphocytes with markers for T-helper cells or in the helper/suppressor ratio. An increase in the expression of HLA-Dr antigen and transferrin receptors was greater when cells were incubated with 13-cRA than with either BC, CTX, or RBG, while carotenoids produced a greater increase in the expression of IL-2 receptors than 13-cRA. Our study indicates that both retinoids and carotenoids might be activating different subpopulations of immune cells.

Adult↗