Showing papers on "Phosphofructokinase activity published in 1978"

Biochemical skeletal muscle and hematological profiles of moderate and severely iron deficient and anemic adult rats.

Abstract: The time course of the effects of moderate and severe iron deficiency anemia on tissue biochemistry of adult male rats was studied. Nine groups of adult male Sprague-Dawley rats were killed; eight of which had approximately 8 g hemoglobin (Hb)/dl (moderately anemic) for 3 to 360 days and one group which had approximately 4 g Hb/dl (severely anemic) for 30 days. Plasma iron was depressed in the mod erately and severely anemic groups at all times relative to nonanemic control rats. Moderately anemic rats at 360 days had a low mean corpuscu lar Hb and mean corpuscular volume and severely anemic rats at 210 days had a low mean corpuscular Hb, and elevated mean corpuscular Hb concen tration. Cytochrome oxidase activity of the white vastus lateralis, red vastus lateralis and soleus muscles were not different between the moderately anemic groups and their respective control groups at any time, but was significantly lower after 30 days of severe iron deficiency anemia. The myoglobin content and phosphofructokinase activity of these muscles showed no significant group differences with moderate or severe iron de ficiency. It is concluded that: 1) moderate iron deficiency anemia imposed no stimulus for alterations of the oxidative or glycolytic capacity of skeletal muscle, whereas severe iron deficiency anemia induced rapid select changes in a mitochondrial component of skeletal muscle, 2) the blood profiles in conjunction with the muscle biochemistry data in the moderately anemic group suggest a hypochromic, microcytic, "manifest iron deficiency" anemia, while those of the severely anemic group suggest a hypochromic, normo- cytic, "severe iron deficiency" anemia. J. Nutr. 108: 1306-1314, 1978.

Post-mortem changes in human central nervous tissue and the effects on quantitation of nucleic acids and enzymes.

Abstract: A study of post-mortem changes in human central nervous tissue has shown that within 100 h of death, no significant change occurs in the amount of nerve cell DNA and nucleolar RNA nor in some membrane-associated enzymes such as succinate dehydrogenase, NADH and NADPH diaphorase, and cytochrome oxidase. Low molecular weight RNA species, probably transfer and messenger RNA are quickly lost, but there is little alteration in ribosomal RNA content. Cytoplasmic enzymes show variable changes; phosphofructokinase activity is rapidly decreased; hexokinase is unaltered but lactate dehydrogenase, pyruvate kinase and glucose-6-phosphate dehydrogenase initially show increases in activity which subsequently decline. Oxygen uptake diminishes quickly. These findings indicate that mechanical alterations in cell structure, following death, render organelles physiologically ineffective long before any significant changes in certain constituent biochemicals are detected. This report emphasizes the great importance necessary in the selection of appropriately time matched post-mortem tissues if accurate comparative studies of many of the cells constituents are to be made.

Familial congenital muscular dystrophy caused by phosphofructokinase deficiency

Abstract: Two children, born to related parents, presented since birth a muscular defect rapidly complicated by painful joint stiffness. The oldest child died at 6 months of age, from respiratory complications. The second-14 month old- does not sit without support. The muscle fibres are of unequal calibre and numerous fibres have under-sarcolemmal PAS positive areas contain glycogen, as seen on electron microscopy. In the second patient, the biochemical analysis showed a moderate glycogen accumulation and muscular enzymatic studies demonstrated an isolated and major deficiency in phosphofructokinase activity. Activity was normal in red blood cells and in fibroblasts cultured in vitro. Hence, these cases should be distinguished from formerly reported cases of phosphofructokinase deficiency. This type of P.F.K. deficiency should be looked for in patients with severe congenital muscular dystrophy and early joint involvement.