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At least 955 records · Page 53Linked to original sources
PubMed1986

Effects of T-2 toxin on induction of petite mutants and mitochondrial function in Saccharomyces cerevisiae.

The influence of the trichothecene mycotoxin T-2 on the mitochondria of Saccharomyces cerevisiae was studied. T-2 is a cytotoxic molecule inhibiting growth and macromolecular synthesis in S. cerevisiae. At low concentrations, T-2 toxin arrested yeast growth on glycerol medium and at higher concentrations, it arrested growth on glucose medium. The toxin was not capable itself of inducing petite mutations. Its inhibitory effect on the growth of petite strains, of both chromosomally isogenic and non-isogenic strains was less than that of grande strains. One exception to this was equally low susceptibility of psi+ SUP4-3 strain in both rho+ and rho- state. T-2 toxin was also capable of retarding the petite inducing activity of the mutagen, ethidium bromide. T-2 toxin inhibited the polymerization of P-ribo-sylaminoimidazole in an ade2 strain of S. cerevisiae. These results show that T-2 toxin is capable of interfering with the activity of the mitochondria in addition to its well studied effects on cytoplasmic protein synthesis.

Cell Division↗
PubMed1994

The use of a water-soluble formazan complex to quantitate the cell number and mitochondrial function of Leishmania major promastigotes.

One of the methods to quantitate Leishmania major promastigotes (LmP) has been to utilize the formation of a formazan dye, which in turn is produced via conversion of an artificial substrate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The method has one major drawback in that the formazan complex precipitates inside the parasites and has to be extracted by denaturants before measurements can be performed. By using a new synthetic substrate, 3-(4,5-dimethylthiazol-2-yl)-5- (3-carboxymethoxyphenyl)-2-(4-sulfonyl)-2H-tetrazolium (MTS), the extraction procedure is eliminated as the formazan-like dye is released spontaneously into the medium, making it possible to perform several measurements on the same parasite culture without disturbing or killing the parasites. The measurements were shown to reflect the numbers of parasites as confirmed via comparative experiments using radioactive thymidine uptake and cell counting, respectively. The method is simple, fast, and highly reproducible and is suitable for drug screening, identification of drug-resistant isolates, and growth-kinetics studies. It is therefore contemplated that the MTS method will be a general and useful technique in this field of parasitology.

Animals↗
PubMed1992

Structural and functional mitochondrial abnormalities associated with high levels of partially deleted mitochondrial DNAs in somatic cell hybrids.

Kearns-Sayre syndrome (KSS) is a progressive and ultimately fatal human encephalomyopathy that is associated with large-scale deletions of mitochondrial DNA (mtDNA). To gain new insights into the developmental pathobiology of this disease, we studied the maintenance and expression of deleted mtDNAs (delta-mtDNAs) in somatic cell hybrids generated by fusion of HeLacot cells with a KSS fibroblast clone containing both wild-type and delta-mtDNAs. We observed that delta-mtDNAs were preferentially maintained over the KSS wild-type mtDNAs (wt-mtDNAs) in almost all isolated hybrid clones. Mitochondrial metabolism was not compromised in hybrids containing as much as 70-79% delta-mtDNAs. Two clones containing more than 99% delta-mtDNA were severely deficient in oxidative phosphorylation and exhibited abnormal, enlarged mitochondria. These clones had undetectable levels of mtDNA-encoded polypeptides, but contained normal amounts of a nuclear DNA-encoded mitochondrial protein. The data suggest a nonrandom pattern of mtDNA segregation in the triplasmic hybrids and a correlation among delta-mtDNA, structural mitochondrial abnormalities, and mitochondrial dysfunction.

Cell Division↗
PubMedDate not supplied

Morphology and mitochondrial function of the surviving myocardium following myocardial infarction in the cat.

The surviving myocardium of the cat was studied 7 days and 6 weeks following experimental infarction. Seven days after infarction, ultrastructural alterations of the mitochondria indicative of slight hypoxic injury--clearing of the matrix and loss of dense matrix granules--were found. Together with intracellular edema and glycogen depletion this result was considered as a sign of relative hypoxia in the surviving myocardium 7 days after infarction. At the same time beta-glucuronidase activity of tissue homogenates was found to be elevated. Focal ischemic lesions in remote myocardium which have been described by other authors (5, 6, 23) were not detected in our experiments. Six weeks after infarction, the fractional volume occupied by myofibrils had increased whereas the fractional volume of mitochondria had remained unchanged (left ventricle) resp. had decreased (right ventricle). There were no qualitative changes detectable at the ultrastructural level. Based on the morphometric investigation of Anversa (1, 2), our results were regarded indicative of mild compensatory hypertrophy of the surviving myocardium. Glutamate dehydrogenase activity of tissue homogenates was shown to be increased when compared to control values. Furthermore our morphometric results showed that the unit mass of mitochondria has to render an enhanced amount of energy six weeks after infarction which might leave the surviving myocardium with a higher susceptibility to future hypoxic injury.

Animals↗
PubMed1994

Inhibition of rat mitochondrial functions in vivo by 6-OHDA and reserpine.

Reserpine caused a decrease in the state 3, respiratory control ratio (RCR) and ADP/O ratio in frontal cortex, striatum and liver of rats 1 h after drug administration. State 4 respiratory rate was stimulated in frontal cortex and striatum. In the liver, 6-OHDA decreased the ADP/O ratio when both pyruvate/malate and succinate were used as substrates. Reserpine induced changes in the activities of Na+K(+)-ATPase and Mg(2+)-ATPase in frontal cortex and liver 15 min and 4 h after administration of the drug. In the liver only 6-OHDA caused the depression of Mg(2+)-ATPase activity (P < 0.05). Reserpine altered the levels of K+, Na+ and Ca2+ cations in rat frontal cortex and striatum, while 6-OHDA caused a decrease in the amount of Mg2+ in liver (P < 0.05).

Animals↗