Sentence examples for mitochondrial functionality in from inspiring English sources

To investigate whether Ret signaling also rescued mitochondrial functionality in Drosophila, we measured ATP content of thoracic homogenates.

Yet, mitochondrial functionality in the intoxicated cell was not improved with EBN treatment in the present study.

To investigate specifically the mitochondrial functionality in Drp/MC muscles, we measured their membrane potential in myofibres from WT and Drp/MC gastrocnemius by using the fluorochrome tetramethyl rhodamine methyl ester (TMRM).

Oxygen consumption rate is reputed to be a good marker of mitochondrial functionality: in fact the decrease of oxygen consumption capability causes the reduction of ATP production so that the cells have to boost anaerobic glycolysis to get ATP from sugars thus increasing glucose consumption and lactate production [ 20].

Introduction: Inhibition of mitochondrial Complex I is described in human and animal sepsis.1,2 This may be responsible, at least in part, for the decrease in mitochondrial functionality seen in sepsis.

For SMDC (sudden mitochondrial deprivation of Ccm1p), complemented Δ ccm1 segregants that carried pCCM1LC or pCCM1ZZLC were initially checked for mitochondrial functionality by growth in the presence of glycerol, ethanol, or lactate as sole source of carbon and energy.

The observed difference in mitochondrial functionality and sarcoplasmic proteome profile suggested existence of intramuscular metabolic variation in bovine semimembranosus.

This compromised mitochondrial functionality was also observed in the marked accumulation of metabolites which are essential for the biosynthesis of nucleotides, in particular glutamine and glycine, suggesting a hindered biosynthesis of purine and pyrimidine nucleotides, a known effect of mitochondrial dysfunction [27], [28].

Our data suggest an intricate connection between polyglutamine-induced toxicity, mitochondrial functionality and iron homeostasis in this model system.

These data show that damages to the mitochondrial system occur in polyglutamine intoxicated yeast cells and suggest an intricate connection between polyglutamine-induced toxicity, mitochondrial functionality and iron homeostasis in this model system.

However, despite a very robust rescue to the ovarian follicle pool, Bax deficiency was not able to restore mitochondrial functionality or correct the choromosomal misalignments in ovulated oocytes, indicating that, in oocytes, Mcl-1 regulates additional aspects of cellular and mitochondrial physiology independent of Bax or cell death.