Reduced triphosphopyridine nucleotide and pyrophosphate-dependent peroxidation of lipids in rat liver microsomes were coupled to the generation of ethylene in the presence of cuprous ions. This system suggests a model for the biogenesis of ethylene in cells.

Adenosine Triphosphate↗

PubMed1966

Actinomycin D: inhibition of respiration and glycolysis.

Actinomycin D inhibited respiration and anaerobic glycolysis of human leukemic leukocytes and lowered the adenosine triphosphate content of the cells. Inhibitory effects on respiration and on RNA synthesis could not be dissociated from one another over a wide range of drug concentrations. Actinomycin D also impaired protein synthesis, probably by decreasing the availability of adenosine triphosphate and by inhibiting messenger RNA.

Adenosine Triphosphate↗

PubMed1964

Evidence for the involvement of iron in the ADP-activated peroxidation of lipids in microsomes and mitochondria.

Explore the source record for details and available documents.

Adenine Nucleotides↗

PubMedDate not supplied

Futile redox cycling: implications for oxygen radical toxicity.

The reduction and the potential autoxidation of quinoid compounds may be viewed as taking place in three cell compartments. In microsomal fractions (endoplasmic reticulum) one-electron reduction by NAPDH-cytochrome P450 reductase leads to the formation of semiquinones which rapidly react with oxygen to form the parent quinone and superoxide anions. The formation of superoxide through this futile cycle leads ultimately to other damaging species (H2O2 and .OH). A similar futile cycle in mitochondria involves NADH dehydrogenase. In this instance, mitochondria initiation of such a cycle with quinones results not only in the formation of toxic radical species but also in the diversion of electrons from phosphorylating pathways. The consequent diminution of cellular ATP may have as important a consequence with respect to the toxicity of quinones as the generation of radicals. Finally, cytosolic DT diaphorase, which carries out a two-electron reduction of quinones to more stable hydroquinones, may compete with the one-electron systems and participate in the detoxification of quinones by supplying hydroquinones for conjugation reactions. The extent of quinone-induced damage may thus vary from cell to cell depending on the integration of these pathways.

Adenosine Triphosphate↗