Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human placental mitochondria prepared by a new isolation procedure exhibit low but well coupled rates of state 3 respiration with different substrates (succinate: 32.3 nmol O2/mg/min, RCI = 4.4; pyruvate: 12.6 nmol O2/mg/min, RCI R = 4.2; palmitoylcarnitine: 16.6 nmol O2/mg/min, RCI R = 4.9). The addition of the uncoupler FCCP increased the respiratory rates (succinate: 40.7 nmol O2/mg/min; pyruvate: 21.2 nmol O2/mg/min: palmitoylcarnitine: 25.4 nmol O2/mg/min). The low respiratory rates correlate well with a low capacity of the respiratory chain as shown by the specific contents of cytochrome c (0.15 nmol/mg), cytochrome b (0.19 nmol/mg) and cytochrome oxidase (0.14 nmol/mg) as well as with the low content of adenine nucleotides (2.71 nmol/mg). These data together with the finding of high activities of alkaline phosphatase (2.2 U/mg) support the view that human placental mitochondria are contaminated with nonmitochondrial membranes. Since it was not possible to obtain functionally intact mitochondria with negligible activities of alkaline phosphatase the influence of this enzyme on the extramitochondrial adenine nucleotide turnover was investigated. Alkaline phosphatase splits phosphate from ATP, ADP and AMP with different rates resulting in an intermediate accumulation of AMP. Mitochondrial adenylate kinase (0.16 U/mg) regenerated ADP from AMP and ATP resulting in drastically decreased ADP/O ratios and prolonged state 3 respirations. Inhibiting the adenylate kinase with diadenosine pentaphosphate the ADP regeneration from AMP and ATP was suppressed which, in turn, enhanced the ADP/O ratios. In the absence of magnesium ions, if both the alkaline phosphatase and the adenylate kinase are inhibited normal ADP/O ratios and state 3-state 4 transitions can be observed. Under these conditions, human placental mitochondria showed normal properties comparable to those of mitochondria from other tissues with the only exception of low specific activities.
Placenta 1994 Apr
PMID:Unusual properties of mitochondria from the human term placenta are caused by alkaline phosphatase. 806 53

In utero exposure of fetuses to tobacco is associated with reduced birth weight. We hypothesized that this may be due to the toxic effect of carbon monoxide (CO) from tobacco, which has previously been described to damage mitochondria in non-pregnant adult smokers. Maternal peripheral blood mononuclear cells (PBMCs), newborn cord blood mononuclear cells (CBMCs) and placenta were collected from 30 smoking pregnant women and their newborns and classified as moderate and severe smoking groups, and compared to a cohort of 21 non-smoking controls. A biomarker for tobacco consumption (cotinine) was assessed by ELISA (enzyme-linked immunosorbent assay). The following parameters were measured in all tissues: mitochondrial chain complex IV [cytochrome c oxidase (COX)] activity by spectrophotometry, mitochondrial DNA levels by reverse transcription polymerase chain reaction, oxidative stress by spectrophotometric lipid peroxide quantification, mitochondrial mass through citrate synthase spectrophotometric activity and apoptosis by Western blot parallelly confirmed by TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labelling) assay in placenta. Newborns from smoking pregnant women presented reduced birth weight by 10.75 percent. Materno-fetal mitochondrial and apoptotic PBMC and CBMC parameters showed altered and correlated values regarding COX activity, mitochondrial DNA, oxidative stress and apoptosis. Placenta partially compensated this dysfunction by increasing mitochondrial number; even so ratios of oxidative stress and apoptosis were increased. A CO-induced mitotoxic and apoptotic fingerprint is present in smoking pregnant women and their newborn, with a lack of filtering effect from the placenta. Tobacco consumption correlated with a reduction in birth weight and mitochondrial and apoptotic impairment, suggesting that both could be the cause of the reduced birth weight in smoking pregnant women.
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PMID:Molecular basis of reduced birth weight in smoking pregnant women: mitochondrial dysfunction and apoptosis. 2518 90