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E Piña

Publications and source records attributed to E Piña.

49 records · Page 3Linked to original sources
PubMedDate not supplied

Effects of moderate chronic ethanol consumption on rat liver mitochondrial functions.

The biochemical consequences of moderate chronic ethanol ingestion has been scarcely investigated in spite of the fact that most of the human population drinks ethanol on a moderate basis. This paper describes some metabolic effects produced by moderate ethanol consumption. The substitution of drinking water in rats for a 10% ethanol solution during 4 weeks resulted in: a) a decrease of blood urea and citrulline synthesis in liver mitochondria; b) a slight inhibition in state 3 and state 4 respiration either with glutamate-malate as substrates or succinate as substrate; c) no change in ADP/O ratio with succinate but slight increase with glutamate-malate; d) a reduction of the cytochrome oxidase activity and cytochromes a+a3 content; e) a 42% increase in the succinate dehydrogenase activity and a small but constant increase in the Vmax (no change in the Km) of the adenine nucleotide translocase activity in liver mitochondria. These results show that even moderate, but continuous ethanol ingestion, produces metabolic responses that must be carefully evaluated to define health risk in larger human groups.

Adenosine Diphosphate↗
PubMedDate not supplied

Importance of age upon the increase in HDL2-cholesterol in the alcoholic.

An inverse relationship has been found between high density lipoprotein cholesterol (HDL-C) and the incidence of coronary disease. A controversy exists in the international literature as to which sub-fraction, HDL2-C or DHL-C, rises after ethanol ingestion. This paper studies a comparison of the levels of circulating cholesterol, HDL-C, HDL2-C and HDL3-C in two groups: a control group of 44 healthy subjects who had no ethanol in over a year, and a second one made up off 40 chronic alcoholics, who consumed between 80 and 160 gr. of ethanol per day. The alcoholic population showed lower levels of cholesterol and higher levels of HDL-C, HDL2-C and HDL3-C. When compared with the control group, the increase was in alcoholics 58% for HDL2-C and 29% for HDL3-C. An analysis of the different age groups shows an increase of 110% in HDL2-C, in alcoholics between ages 31 and 40, as compared with their control group. An increase of 81% occurred between ages 51 and 60, but rarely rose 20% between ages 21 and 30, as well as between 51 and 60. The maximum rise of HDL3-C in drinkers, related to their control group, was 38% during the fourth decade of life. The conclusion is that the HDL2-C subfraction rises in chronic alcoholics, and the changes in other HDL-C subfractions are more useful when they are placed at the different individual's decades of age, than when taken from complete population samples.

Adult↗