acidosis/protease

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Highly active antiretroviral therapy (HAART)-associated lactic acidosis: in vitro effects of combination of nucleoside analogues and protease inhibitors on mitochondrial function and lactic acid production.

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Lactic acidosis is a rare but potentially life-threatening and poorly understood sequelae among HIV-infected patients on highly active antiretroviral therapy (HAART). Mitochondrial DNA depletion and inhibition of respiratory complexes have been hypothesized to be involved in HAART-associated lactic

Defective mitochondrial protease LonP1 can cause classical mitochondrial disease.

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LonP1 is a mitochondrial matrix protease whose selective substrate specificity is essential for maintaining mitochondrial homeostasis. Recessively inherited, pathogenic defects in LonP1 have been previously reported to underlie cerebral, ocular, dental, auricular and skeletal anomalies (CODAS)

[Lactic acidosis type B. A life-threatening adverse effect of antiretroviral therapy].

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A thirty-year old HIV-positive woman, who had been receiving antiretroviral therapy (protease inhibitor, lamivudine and stavudine) for seven months, was diagnosed with severe lactic acidosis type B, most likely induced by nucleoside reverse transcriptase inhibitor treatment. The antiretroviral

Regulation of the insulin-like growth factor system by acute acidosis.

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Many catabolic conditions are characterized by disturbances in acid-base balance and concomitant alterations in the insulin-like growth factor (IGF) system. However, the influence of acidosis per se on the various components of the IGF system has not been extensively examined. The purpose of the

Mechanisms for protein catabolism in uremia: metabolic acidosis and activation of proteolytic pathways.

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Accelerated protein catabolism in uremia occurs in animals and patients with acute (ARF) and chronic renal failure (CRF). Possible causes include resistance to both insulin-induced inhibition of protein-degradation and insulin-induced stimulation of protein synthesis. The mechanisms for these

Use of protease inhibitor (trasylol) and heparin in cardiorespiratory resuscitation. II. Gasometric investigations of arterial blood.

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The purpose of the present work was to assess the effect of trasylol--an inhibitor of proteases--and heparin on gasometric values in arterial blood during cardio-respiratory resuscitation. The investigations were carried out on rabbits in three experimental groups. In group I the simplest

Acidosis regulates the stability, hydrophobicity, and activity of the BH3-only protein Bnip3.

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Bnip3 is a prodeath member of the so-called BH3-only subfamily of Bcl-2 proteins. A major function of this class of proteins is to regulate the permeability state of the outer mitochondrial membrane by forming homoand hetero-oligomers inside the membrane. We reported previously that Bnip3

Trafficking defects of a novel autosomal recessive distal renal tubular acidosis mutant (S773P) of the human kidney anion exchanger (kAE1).

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Autosomal dominant and recessive distal renal tubular acidosis (dRTA) can be caused by mutations in the anion exchanger 1 (AE1 or SLC4A1) gene, which encodes the erythroid chloride/bicarbonate anion exchanger membrane glycoprotein (eAE1) and a truncated kidney isoform (kAE1). The biosynthesis and

Identification of proteasome gene regulation in a rat model for HIV protease inhibitor-induced hyperlipidemia.

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Patients treated with highly active antiretroviral therapy may develop metabolic side effects such as hyperlipidemia, insulin resistance, lipoatrophy and lactic acidosis. The pathophysiology of these metabolic abnormalities is unknown, although some, e.g., lactic acidosis and lipoatrophy, are more

Acidosis-induced apoptosis in human and porcine heart.

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BACKGROUND Acidosis-mediated injury to cardiac myocytes during surgery may lead to progressive heart failure. The nature of this injury, although not well defined, may be caused by induction of apoptosis in cardiac myocytes. We applied fluorescence imaging and biochemical techniques to assess

Lactic acidosis secondary to nucleoside analogue antiretroviral therapy.

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A 53-year-old woman with newly diagnosed HIV infection was treated with the nucleoside analogue antiretroviral agents lamivudine and stavudine and the protease inhibitor indinavir. An illness characterized by severe lethargy, persistent nausea and vomiting, lactic acidosis, hyperglycemia, and

Therapeutic regimens in acute experimental hemorrhagic pancreatitis. Effects of hydration, oxygenation, peritoneal lavage, and a potent protease inhibitor.

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In this study we evaluated the effects of hydration, oxygenation, peritoneal lavage, and the protease inhibitor gabexate mesilate in acute hemorrhagic pancreatitis induced by feeding mice a choline-deficient, ethionine-supplemented diet. Different groups of mice were kept at various concentrations

Acidosis, magnesium and acetylsalicylic acid: effects on thrombin.

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Thrombin, an enzyme from the hydrolase family, is the main component of the blood coagulation system. In ischemic stroke it acts as a serine protease that converts soluble fibrinogen into insoluble strands of fibrin forming blood clots in the brain. It has been found to phosphoresce at room

Hepatic steatosis and lactic acidosis caused by stavudine in an HIV-infected patient.

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Lactic acidosis and hepatic steatosis caused by mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTI) is a rare cause of liver disease with a high mortality rate. This report describes a male, HIV-positive patient with a 4-week history of nausea, vomiting and abdominal pain.

Release of cellular proteases into the acidic extracellular milieu exacerbates Ebola virus-induced cell damage.

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Ebola virus is highly cytopathic through mechanisms that are largely unknown. We present evidence that progressive acidification of the extracellular milieu by Ebola virus-infected cells combined with reduced levels of natural cysteine protease inhibitor makes the cells vulnerable to uncontrolled

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