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PubMed1970

Effects of heat treatment of electron-transport particles on bacterial oxidative phosphorylation.

The electron-transport particles from Mycobacterium phlei exhibit low levels of phosphorylation unless supplemented with soluble coupling proteins. Heat treatment of the electron transport particles for 15 min at 50 degrees C was found to result in a slight loss of oxidation and an activation of phosphorylation with NADH as substrate, while with succinate as substrate both activities increased. The heat-activated particles do not require the addition of soluble coupling factors and their level of oxidative phosphorylation is similar to that of the regular particles supplemented with the soluble coupling factors. In contrast to the lack of a requirement for the soluble coupling factors after heat activation, the heat-treated electron-transport particles require the presence of a particulate-bound coupling factor for phosphorylation. The heat-activated system, like the untreated system, was found to be sensitive to uncoupling agents.

Adenosine Triphosphatases↗
PubMed1997

Rate of oxidative phosphorylation in isolated mitochondria from human skeletal muscle: effect of training status.

Muscle oxidative function has been investigated in subjects with various training status (VO2 max, 41-72 mL O2 kg-1 body wt min-1, n = 10). Mitochondria were isolated from biopsies taken from m. vastus lateralis. Maximal mitochondrial oxygen consumption (QO2) and ATP production (MAPR) were measured with polarographic and bioluminometric techniques, respectively. The yield of mitochondria, calculated from the fractional activity of citrate synthase (CS), averaged 26%. With pyruvate + malate, the respiratory control ratio was 5.7 +/- 0.4 (X +/- SE) and the P/O ratio was 2.83 +/- 0.02, which demonstrates that the isolated mitochondria were functionally intact. QO2 was significantly correlated to aerobic training status expressed as muscle CS activity (r = 0.86), VO2 max (r = 0.84) and lactate threshold (r = 0.83) but not to the fibre type composition. A highly significant correlation (r = 0.93) was observed between ATP production calculated from QO2 and MAPR, but ATP production derived from QO2 was higher than MAPR both for pyruvate + malate (255%) and for alpha-ketoglutarate (23%). QO2 extrapolated to a temperature of 38 degrees C averaged 68 mL O2 min-1 kg-1 wet wt, which is similar to previous findings in vitro and in vivo during the post-exercise period. However, calculated muscle O2 utilization during exercise was three- to fivefold higher than QO2 measured on isolated mitochondria. It is suggested that additional factors exist for activation of mitochondrial respiration during exercise. It is concluded that muscle oxidative function can be quantitatively assessed from the respiration of mitochondria isolated from needle biopsy specimens and that QO2 is closely correlated to whole-body VO2 max.

Adenosine Triphosphate↗
PubMed2000

[Oxidative phosphorylation defects with neonatal presentation: review of our caseload].

OBJECTIVES: To define the oxidative phosporilation deficit syndrome in the neonatal in terms of incidence and clinical, biochemical and genetic features. MATERIAL AND METHODS: We report 9 newborns diagnosed as oxidatic phosporilation deficit during the last 8 years in our hospital by means of clinical, metabolic, pathological and molecular studies, among other evaluations. The diagnosis was established based on ensymatic deficit of the respiratory chain, associated with alterations in the mtDNA in one case, and with mitochondrial ultrastructural anomalies in 5 cases. RESULTS: There was an incidence of 1/3.555 newborns and 1/832 newborns admitted in our Neonatal Unit. In four of them there were familial antecedents and polihidramnios in two. Most of them, 8 out of 9, were born at term after a normal pregnancy and delivery, with normal Apgar score and auxological examination. Symptomatology started immediately at the neonatal period as acute neurological damage in most of them. There was a severe evolution as 5 children died and 4 survived with severe damage. All of them had the classical phenotype of early severe encefalopathy, associated with dismorphic features, hypotomía, neurosensorial defects, brain dysgenesis and atrophy, anomalies in the EEG and in 5 of them there were also systemic anomalies, mainly cardiopathy. The most frequent biochemical alteration was a significative increment of the quotient lactate/piruvate. Five patients presented ultrastructural alterations of the mitochondria in thr muscle biopsy but Cox stain was not positive in any case. Three cases has a deficit of the complex IV, e of the complex I-IV, 2 of the complex I and one the complex I-III-IV. Only one patient had multiple deletions in the mtDNA. CONCLUSIONS: Oxidatic phosporilation deficit are frequent and severe diseases of prenatal onset with limited fetal effects, homogeneous clinical phenotype with frequent damage of the central nervous system and variable extraneurological alteration and inconsistent biochemical pattern. Enzymatic studies ar need for making the diagnosis in all suspected cases,

Female↗