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PubMed1975

The role of mitochondria in the contraction-relaxation cycle and other Ca2+-dependent activities of heart cells.

The problem of whether mitochondria participate in the contraction and relaxation of heart by binding Ca2+ reversibly has been discussed actively in recent times. The role of mitochondria has not yet been conclusively established, but is suggested by several lines of evidence, particularly in amphibian hearts. Apart from contraction and relaxation, the Ca2+ transport system of mitochondria may influence many Ca2+-sensitive cell reactions. Some are mitochondrial (succinate oxidase, alpha-glycerophosphate dehydrogenase, pyruvate dehydrogenase phosphate phosphatase) and may control the operations of the respiratory chain and of the trichloroacetic acid cycle. Among the extramitochondrial Ca2+-sensitive reactions are phosphorylase b kinase, phospholipases, and pyruvate kinase. The latter activity has been studied in detail, and it has indeed been found that it can be modulated by mitochondria. It appears possible that the mitochondrial system for binding and transporting Ca2+ is an efficient means to regulate various phases of cell metabolism.

Animals↗
PubMed1992

Glycogen storage disease diagnosed in adults.

Glycogen storage diseases are usually identified in childhood. We present the clinical, biochemical and histological features of 10 patients first diagnosed in adult life. Five had glycogen storage disease type 1a, one type 1c, two type IX, and in two patients there were previously unreported abnormalities of hepatic glucose-6-phosphatase system activity. Of the latter, one patient had an inhibitor of liver glucose-6-phosphatase (pseudo-1b glycogen storage disease) the other having abnormal glucose-6-phosphatase activity and microsomal pyrophosphate transport. A glucagon test is suggested as a useful screening procedure. Glycogen storage disease should be considered in adults with symptoms suggesting hypoglycaemia.

Adolescent↗
PubMed1991

The mechanism of organ injury in alcoholics: implications for therapy.

Organ damage due to alcohol abuse includes especially the CNS and the GI tract. The mechanism of liver injury has been studied in depth. Alterations in membrane fluidity, signal transduction, cytochrome, P-450 induction, oxidative stress, acetaldehyde adducts, eicosanoid metabolism, cytoskeletal function, energy metabolism, O2 consumption, microcirculation, Kupffer cell and ito cell activation, immune injury, and gene expression have been documented. Therapeutic implications of these studies include oxandrolone, PTU and colchicine. Pancreatic injury has been studied in vivo and with isolated acini. Amylase release is enhanced directly by ethanol probably by increasing cytosolic Ca2+. Chronic alcohol feeding decreases the CCK receptor sensitivity and affinity for CCK and the pkc response is reduced as is Ca2+ mobilization. Eicosanoids may mediate the damage to the gastric microcirculation. Inhibitors of leukotriene A4 synthesis reduce the ethanol-induced mucosal damage. Exogenous prostaglandins protect the gastric mucosa from ethanol damage and microvascular stasis. In the CNS, alterations induced by ethanol include changes in membrane fluidity and receptor transduction modulation.

Alcoholism↗
PubMed1989

Disorders of glycogen metabolism of muscle.

Glycogen is a crucial source of energy in the initial stages of muscle activity and during exercise of high intensity. There are 10 well-defined biochemical defects of glycogen metabolism expressed in muscle and affecting the following enzymes: alpha 1,4 glucosidase (glycogenesis type II), debrancher enzyme (III), brancher enzyme (IV), phosphorylase (V), phosphofructokinase (VII), phosphorylase b kinase (VIII), phosphoglycerate kinase (IX), phosphoglycerate mutase (X), lactate dehydrogenase (XI). These disorders cause two main syndromes: one characterized by exercise intolerance with cramps and myoglobinuria, the other by fixed weakness. However, there are examples of clinical and biochemical heterogeneity for each disease, and molecular genetic analysis is already showing evidence of genetic heterogeneity. Although our understanding of the biochemical errors has progressed considerably, the pathogenesis of symptoms and signs remains incomplete.

Enzymes↗
PubMed1985

The role of phosphorylations in the regulation of ion fluxes.

Ions appear as very important second messenger since steep ionic gradients are established between subcellular compartments as well as between the outside and the inside of the cell and ions are very diffusible molecules. Ions have been shown to induce many biological events as exemplified by the triggering of skeletal muscle contraction by calcium ions. There is more and more evidence that the same ions might play as tuning systems for biological functions. Therefore their concentration must be precisely controlled. This paper summarizes evidences that phosphorylation of regulatory proteins modulates the cytoplasmic level of some ions.

3',5'-Cyclic-AMP Phosphodiesterases↗