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D J Tuma

Publications and source records attributed to D J Tuma.

165 records · Page 10Linked to original sources

Betaine effects on hepatic methionine metabolism elicited by short-term ethanol feeding.

Previous studies in this laboratory have shown that feeding of ethanol to rats produces prompt inhibition of methionine synthetase (MS) as well as a subsequent increase in activity of betaine homocysteine methyltransferase (BHMT). Further studies have shown that supplemental dietary betaine enhanced methionine metabolism and S-adenosylmethionine (SAM) generation in control and ethanol-fed rats. Because MS and BHMT are both involved in the formation of SAM, this study was conducted to determine early effects of ethanol on hepatic SAM levels and the influence of betaine supplementation on parameters of methionine metabolism during the early periods of MS inhibition and enhanced BHMT activity. Results showed that ethanol feeding produced a significant loss in SAM in the first week with a return to normal SAM levels in the second week. Betaine feeding enhanced hepatic betaine pools in control as well as ethanol-fed animals. This feeding attenuated the early loss of SAM in ethanol-fed animals, produced an early increase in BHMT activity, and generated increased levels of SAM in both control and ethanol-fed groups. Furthermore, betaine lowered significantly the accumulation of hepatic triglyceride produced by ethanol after 2 weeks of ingestion.

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Effects of cytochalasin B on the synthesis and secretion of plasma proteins by developing rat liver.

Antimicrotubular drugs such as colchicine impair plasma protein secretion markedly less from developing liver than from mature tissue, suggesting the reduced participation of microtubules in hepatic protein secretion during liver development. In order to evaluate the possible contribution of microfilaments to protein export by immature liver, we incubated slices prepared from adult and gestation day 19 fetal rat liver for up to 4 h with the antimicrofilamentous agent cytochalasin B and with colchicine in various concentrations. In adult tissue, cytochalasin B did not reduce either the synthesis or secretion of [14C]leucine-labeled proteins and albumin. Cytochalasin B decreased apparent albumin synthesis by fetal liver, but otherwise, its effects on [14C]leucine incorporation did not differ from those observed in the adult. In contrast with leucine, the uptake of [3H]glucosamine into both adult and fetal liver was reduced by cytochalasin B. When this reduced uptake was normalized to that in corresponding control incubations, [3H]glucosamine incorporation into glycoproteins was markedly diminished in fetal slices, but was unaffected in the adult. Despite this age-dependent difference, cytochalasin B only minimally affected glycoprotein secretion in each group. Cytochalasin B never modified the antisecretory effects of colchicine. These results suggest that during early development, liver protein synthesis is more sensitive to toxic effects of cytochalasin B than during adulthood. However, microfilaments are not required for plasma protein export at either time.

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