Biomedical subjects

J Popinigis

Publications and source records attributed to J Popinigis.

At least 19 recordsLinked to original sources

PubMed1992

Effects of alkyl alcohols and related chemicals on rat liver structure and function. III. Physiochemical properties of ethanol-, propanol- and butanol- treated rat liver mitochondrial membranes.

The physicochemical properties of mitochondria in liver tissue obtained from rats given 32% ethanol, 32% propanol or 6.9% butanol in drinking water for up to 3 months were investigated using differential scanning calorimetry and fluorescence polarization measurements. The results obtained were as follows: 1) Phospholipids extracted from mitochondria showed increases in the relative amounts of phosphatidylcholine, phosphatidylinositol and phosphatidylserine, and a decrease in the relative amount of phosphatidylethanolamine. An increase in the unsaturated/saturated fatty acid ratio of phospholipids was also observed. 2) Elevation of the thermotropic lipid phase transition temperature with a decrease in the enthalpy value (delta H) was revealed by differential scanning calorimetry. 3) The elevation of the lipid phase transition temperature was detected also by fluorescence polarization measurements using 1,6-diphenyl-1,3,5-hexatriene (DPH) as a probe. Elevation of mitochondrial membrane fluidity was found in some of the experimental animals, but most showed no changes in comparison with the control. A possible role of membrane fusion in the mechanism of formation of ethanol-, propanol- and butanol-induced hepatic megamitochondria is discussed on the basis of these results.

1-Propanol↗

PubMed1991

Effects of alkyl alcohols and related chemicals on rat liver structure and function. I. Induction of two distinct types of megamitochondria.

The effects of alkyl alcohols and related chemicals on the ultrastructure of mitochondria in the rat hepatocyte were studied. The following three different groups of chemicals were tested: Group 1: alkyl alcohols with straight carbon chains (ethanol, 1-propanol, 1-butanol, 1-pentanol, 1-octanol, 1-dodecanol and 1-octadecanol); Group 2: tert- and cyclo-compounds (tert-butanol, cyclo-pentanol, and cyclo-hexanol); and Group 3: polyhydroxy alcohols (ethylene glycol, propylene glycol, 1, 3-propanediol, glycerol and pentaerythritol). Results obtained were summarized as follows: 1) Ethanol, 1-propanol, 1-butanol, 1-pentanol and 1-octanol had essentially the same effects on the mitochondrial ultrastructure: a mixed population of small and enlarged mitochondria with poorly developed cristae; 1-dodecanol induced ultrastructural changes of mitochondria of two distinct types: a mixed population of small and enlarged mitochondria with poorly developed cristae in some hepatocytes and remarkably enlarged mitochondria with well-developed cristate in others; and 1-octadecanol induced remarkably enlarged mitochondria in all hepatocytes. 2) Chemicals belonging to group 2 and group 3 induced essentially the same changes as those induced by 1-octadecanol. More than one month was required to induce those changes. The mechanism by which those ultrastructural mitochondrial changes were induced is not clear, but the present results may suggest that the hydroxy group (-OH) common to all these chemicals in some way accounts for the phenomenon.

1-Butanol↗

PubMed1991

Effects of alkyl alcohols and related chemicals on rat liver structure and function. II. Some biochemical properties of ethanol-, propanol- and butanol-treated rat liver mitochondria.

Functional changes of mitochondria in the liver obtained from rats given 32% ethanol, 32% propanol and 6.9% butanol in drinking water for up to 3 months were investigated. Animals were also fed a liquid diet containing ethanol for comparison. Results obtained were as follows: 1) Animals given ethanol in drinking water consumed twice as much ethanol daily as those fed a liquid diet containing ethanol, while ultrastructural changes of hepatic mitochondria were essentially the same between the former and the latter animals: the co-existence of megamitochondria and small mitochondria with poorly developed cristae. 2) Effects of alkyl alcohols tested on the respiratory rates and coupling efficiency of mitochondria were variable, depending on the kind of alkyl alcohols, the duration of experiments and oxidizable substrates used. 3) There was essentially no difference between the heavy and the light mitochondrial fractions obtained from alkyl alcohol-treated rat livers in terms of respiratory rates and coupling efficiencies. 4) Decreases in the content of cytochrome aa3 and the activity of activity of cytochrome oxidase, and increases in MEOS activity were most distinct in ethanol-treated rat livers. A possible role of chronic relative oxygen deficiency inside the hepatocyte caused by the metabolization of alkyl alcohols is discussed in order to interpret such peculiar ultrastructural changes of mitochondria.

1-Propanol↗

PubMed1991

Tightly coupled respiration in rat brain homogenates.

"Respiratory control", a typical feature of well coupled mitochondria, was found to be higher in rat brain homogenate than in isolated mitochondria. This observation points to the possibility of studying the coupling between respiration and ADP phosphorylation, as well as mitochondrial metabolism, directly in homogenates and not in isolated mitochondria, using very small samples of brain tissue.

Adenosine Diphosphate↗

PubMed1991

Human skeletal muscle: participation of different metabolic activities in oxidation of L-lactate.

The pure mitochondrial fraction obtained from human skeletal muscle did not show coupled L-lactate (+ NAD) oxidation, but this function could be restored by addition of LDH. Thus the "direct", coupled oxidation of L-lactate described earlier (Popinigis et al., 1990. International Perspectives in Exercise Physiology, Human Kinetics Books, pp. 132-133) should be attributed to contaminations.

Electron Transport↗

PubMed1990

Direct oxidation of glutamate by mitochondria from porcine adrenal cortex.

1. Mitochondria isolated from porcine adrenal cortex under State 3 conditions oxidized succinate with a rate of 47 +/- 4.48 na oxygen/min/mg/protein and with ADP:O ratio 0.98 +/- 0.09. In the presence of 15 microM deoxycorticosterone the rate of succinate oxidation was 36.8 +/- 3.08 na oxygen/min/mg/protein. 2. Under the same conditions the rate of glutamate oxidation was 22.8 +/- 2.21 and 16.8 +/- 0.65 na oxygen/min/mg/protein, respectively. ADP:O ratio was 1.45 +/- 0.14. 3. Introduction of trace amounts of malate into the mitochondria oxidizing glutamate only slightly increased the rate of O2 uptake. 4. The glutamate dehydrogenase activity in these mitochondria was 12.5 +/- 0.69 nmol/min/mg.

Adrenal Cortex↗

PubMed1987

Changes in physicochemical properties of mitochondrial membranes during the formation process of megamitochondria induced by hydrazine.

Changes in some biochemical and physico-chemical properties of rat liver mitochondrial membranes during the formation process of megamitochondria induced by hydrazine were analyzed. Hepatic mitochondria obtained from rats placed on a 1% hydrazine diet for 3 days became slightly enlarged and sometimes elongated, while they became gigantic after 7 days of hydrazine intoxication. Changes were observed in mitochondria from rats treated with hydrazine for 3 days. Total amounts of phospholipids extracted from mitochondria and submitochondrial fractions were increased. Among phospholipid species, relative amounts of acidic phospholipids were increased. Contents of Ca2+ in mitochondria were increased. Differential scanning calorimetric analysis of mitochondria, especially that of the outer membrane fraction, showed that the thermotropic lipid phase transition temperatures were elevated accompanying the broadening of thermograms and the increase in transition enthalpy. Contents of water in mitochondria were increased significantly with the ratio of freezable water to unfreezable water unchanged. Among the changes observed was that the total amount of phospholipids (except for that of the outer membrane fraction) and the contents of water and Ca2+ nearly returned to normal in megamitochondria after 7 days of hydrazine intoxication. Relative amounts of phospholipids and thermotropic lipid phase transition temperatures of megamitochondria did not return to normal levels and yet changes were smaller than those obtained from 3 days of hydrazine intoxication. The fluidity of mitochondrial membranes was not affected by hydrazine treatment. These data would suggest that hydrazine-induced megamitochondrial formation is not due simply to the swelling of mitochondria, but might be due to the fusion of adjacent mitochondria by Ca2+-acidic phospholipid interactions, and once megamitochondria are formed the mitochondrial membranes are stabilized.

Animals↗

PubMed1984

Transaminative pathway of glutamate oxidation in adrenal-cortex mitochondria.

Mitochondria isolated from adrenal cortex of beef do oxidize glutamate if the amino group acceptor-oxaloacetate (or its precursor-malate) is present in the incubation medium. The glutamate (plus oxaloacetate) oxidation was enhanced by ADP or deoxycorticosterone, indicating that this respiration can support both oxidative phosphorylation and 11 beta-hydroxylation of deoxycorticosterone to corticosterone. Avenaciolide (inhibitor of glutamate entry into the mitochondria), aminooxyacetate (inhibitor of aspartate aminotransferase activity) and arsenite (inhibitor of 2-oxoglutarate dehydrogenase) when introduced into the incubation media before respirating substrates, inhibited the ability of ADP or deoxycorticosterone to stimulate the rate of glutamate (plus oxaloacetate) oxidation.

Adrenal Cortex↗

PubMed1979