Biomedical subjects

M L Chang

Publications and source records attributed to M L Chang.

72 records · Page 4Linked to original sources

PubMed1978

Effect of dietary vitamin E and vitamin C on respiration and swelling of guinea pig liver mitochondria.

The effect of dietary vitamin C on vitamin E status and function was studied with weanling male Hartley guinea pigs. Thirty guinea pigs fed a basal diet free of vitamins E and C were divided into two groups; only one group received 2 mg/100 g body weight/day of vitamin C. Each group was further divided into three subgroups and received 0, 0.2, and 0.4 IU/100 g body weight/day of vitamin E. After 5 weeks the animals were killed. Degree of erythrocyte hemolysis induced by dialuric acid, level of plasma vitamin E and extent of liver lipid peroxidation were determined. Liver mitochondria were isolated and in vitro oxygen uptake was measured. The rate of swelling of mitochondria in two media was also determined. The results showed that the adequate dietary vitamin C supplementation did not affect the extent of erythrocyte hemolysis induced by dialuric acid, but increased the plasma vitamin E level and lowered liver lipid peroxidation. It also maintained the normal respiration and swelling rates of liver mitochondria when vitamin E was inadequate.

Animals↗

PubMed1977

Biological behavior of higher molecular weight products of fibrinolysis.

We have examined the consequence of infusions into rabbits of the products of limited plasmin hydrolysis of fibrin (early fibrin degradation products, or early fdp) containing defined quantities of fibrin fragment X. For comparison, early fibrinogen degradation products (early FDP) and late fibrin degradation products (late fdp) consisting almost exclusively of core fragments D and E were infused into separate groups of animals. Components of early fdp, probably fibrin fragment X, behaved in many respects like fibrin monomer. Infused unlabeled early fdp produced circulating soluble fibrin complexes with 125I-labeled fibrinogen. 125I-labeled early fdp rapidly accumulated in the spleen and liver and also to a significant degree in the lungs as insoluble, nonextractable tissue-bound protein; in contrast, only minimal quantities of early FDP and late fdp accumulated in organs. When 125I-labeled early fdp were administered to animals given continuous infusions of epsilon-aminocaproic acid to block fibrinolysis, substantial amounts of radioisotope also accumulated in the kidneys. These observations suggest a possible pathophysiological role for the products of lysing fibrin encountered in clinical states associated with disseminated intravascular coagulation.

Aminocaproic Acid↗

PubMed1976

Analysis of soluble fibrin complexes by agarose gel chromatography and protamine sulfate gelation.

The molecular makeup of soluble fibrin complexes was studied by gel exclusion chromatography using radio-labelling to characterize individual components in protein mixtures. Products of limited plasmin degradation of fibrinogen and mixtures of fibrinogen and "early" fibrinogen digests formed high molecular weight soluble fibrin complexes upon incubation with thrombin. Purified, nonclottable fragment Y did not incorporate into soluble fibrin complexes, nor could we demonstrate incorporation of fragments D and E as previously described from our laboratory. Thus, under the conditions of these experiments, soluble fibrin complexes have two identifiable components, fibrin monomer and clottable fragment X monomer, although incorporation of native fibrinogen or fragment X unreacted by thrombin into soluble fibrin complexes cannot be excluded. Individual fractions of thrombin-treated early fibrinogen digests isolated by agarose gel chromatography were treated with protamine sulfate at 37 degrees C resulting in precipitation-gelation of greater than 90 per cent of high molecular weight soluble fibrin complexes; whereas, less than 10 per cent of lower molecular weight fibrinogen degradation products precipitated by protamine sulfate. These findings do not support the widely held concept that soluble fibrin complexes incorporate nonclottable degradation products of fibrinogen proteolysis, nor do they support the notion that the so-called paracoagulation reaction induced by protamine sulfate results from the splitting of complexes between fibrin monomer and nonclottable fibrinogen degradation products.

Binding Sites↗

PubMed1976

Stoppage of glycogenesis and "over-shoot" of induction of lipogenesis and its related enzyme activities in the liver of fasted-refed rats.

To elucidate the causes of changes of carbohydrate metabolic pathways, the time course of utilization of dietary [U-14C]sucrose and induction of enzyme activities in the livers of rats were investigated. Adult male rats of BHE strain were refed after a fast of 2 days. The nutritionally complete refeeding diet contained 60% sucrose as the only source of carbohydrate. [U-14C]Sucrose was included in the diet on either day 1 or day 2, or both of refeeding. During the first day of refeeding, the radioactivity was incorporated mainly into liver glycogen which rose to over 100 mg/g. During the second day, little 14C appeared in the liver glycogen, which decreased sharply while glucose-6-phosphatase activity increased. The glycogenic pathway thus appeared to be blocked. On the other hand, 14C incorporation in the liver fat was minimal during the first day, but was quite extensive during the second day of refeeding. The enhanced lipogenesis was accompanied by large increases of activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADP-malic dehydrogenase. Results clearly indicate that the carbohydrate load in the liver of intact animals was initially metabolized by the glycogenic pathway. When glycogenesis stopped, carbohydrate was metabolized differently. The enhanced incorporation of [U-14C]sucrose into liver lipids indicates an increased formation of acetyl CoA and an accelerated formation and use of NADPH, probably from increasing dehydrogenase activities. Our data suggest that the blockage of synthesis of glycogen with the continuation of carbohydrate load was a primary cause in over-shooting induction of hepatic dehydrogenase activities and lipogenesis.

Adipose Tissue↗

PubMed1976

Influence of fat level and type of carbohydrate on the capacity of pectin in lowering serum and liver lipids of young rats.

The effect of pectin on lowering cholesterol and fat concentration in tissues of the rat was investigated in relation to the level of fat and the type of carbohydrate. Groups of rats were fed nutritionally complete diets containing equal protein: energy, varied with 5% (low-fat, 2% corn oil plus 3% beff tallow) or 20% (high-fat, 2% corn oil plus 18% beef tallow) fat and cornstarch or sucrose as carbohydrate for 2 weeks. Although there were no interactions, the feeding of pectin reduced the cholesterol level in liver and serum from dietary cholesterol to a greater degree in rats fed the low-fat than in those fed the high-fat diet. This effectiveness also varied with type of carbohydrate. In the low-fat diet, this effectiveness was higher with sucrose than with cornstarch, but in the high-fat diet, it was reversed. The size of perirenal fat pads and the concentrations of total liver lipid and cholesterol were less in rats fed the high-fat pectin diet than in those fed the high-fat diet without pectin, indicating that pectin also had an ability to lower fat absorption. When the level of serum alkaline phosphatase was lowered, pectin was more effective in lowering cholesterol level. This phenomenon, however, seemed due to the type of carbohydrate and fat rather than the cholesterol in the diet. Dietary cholesterol had no effect on the size of perirenal fat pads, but increased liver lipid content greatly in rats fed the high-fat diet. Dietary pectin increased the rate of removal of serum cholesterol, and a similar trend was shown in liver cholesterol which had accumulated from the pre-fed hyper-cholesterol diet.

Adipose Tissue↗

PubMed1974