Martha Zentella de Piña, M.Sc.

martha@laguna.fmedic.unam.mx

Isolation of immunophagocytosis inducing proteins. Experimental intoxication with ethanol

OBJECTIVES

To become acquainted with cell damage by ethanol mechanisms and the possibilities of reverting it with the use of substances that trap the toxic radicals produced or increase cell antioxidant defenses.

SUMMARY

Alcoholism is a health problem in Mexico and the world. The sequence of events that unleash liver disease are not yet known. In our laboratory, we have acute and chronic alcoholic intoxication models with which to study the damage mechanism. Furthermore, early indicators of cell damage have been detected in patients (1.2). We have also studied some substances that can revert or halt the pathological process induced by the exaggerated or prolonged consumption of ethanol. These include anti-inflammatory drugs that attenuate the fatty liver and the accompanying increase in lipid peroxidation (3.4). We have also been able to measure glutathione in the livers of rats treated with ethanol as an index of antioxidant cell defenses and it has been possible to increase its content in the livers of rats treated with ethanol and anti-inflammatory drugs at the same time (5).Due to the knowledge obtained on the influence of cholesterol on ischemic cardiopathy and other vascular ailments, there has been a change over several decades in fat consumption from animal fat, like lard and dripping, to corn and safflower oils, principally. The content of unsaturated fatty acids, especially linoleic acid, is high in these edible oils and gives a predisposition to greater peroxidation. In our model of the animal with acute ethanol intoxication, the influence has been studied of different types of lipids in normolipid and hyperlipid diets. It can be said that rats fed for 4 weeks with normolipid diets based on saturated fats develop less liver fat induced by the exaggerated consumption of ethanol and manage better the free radicals measured as reactive species with thiobarbituric acid.

BIBLIOGRAPHY

1. Martha Zentella de Piña, Aída Hernández-Tobías, Yolanda Saldaña-Balmori, Armando Díaz-Belmont and Enrique Piña. (1992) Biochemical ethanol effects affected by a non-steroidal anti-inflammatory drug. FEBS Letters 298: 123-125.
2. Martha Zentella de Piña, Yolanda Saldaña-Balmori, Aída Hernández-Tobías and Enrique Piña (1993) Nonsteroidal Antiinflammatory Drugs Lower Ethanol-Mediated Liver Increase in Lipids and Thiobarbituric Acid Reactive Substances. Alcohol. Clin Exp Res 17:1228-1232.
3. M. Zentella de Piña, S. Corona, A.E. Rocha-Hernández, Y. Saldaña Balmori, G. Cabrera and E. Piña. (1994) Restoration by piroxicam of liver glutathione levels decreased by acute ethanol intoxication. Life Sci 54: 1433-1439.
4. Martha Zentella de Piña, Armando Díaz Belmont, Lucelly Rodríguez Lizárraga, Sergio Corona García. (1994) Lipoperoxidación de las membranas de eritrocito como un posible indicador del estrés oxidativo en el paciente alcohólico. Rev. Méd. Hospital Gral. 57:15-21.
5. Martha Zentella de Piña, Armando Días Belmont, Lucelly Rodríguez Lizárraga, Alma Rocha Hernánez, Sergio Corona García. (1995) Glutatión sanguíneo en el paciente alcohólico con hepatopatía. Rev. Méd. Hospital Gral. 58:52-58.

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