1,721,005 research outputs found
ACETYL-L-CARNITINE INCREASES CYTOCHROME-OXIDASE SUBUNIT-I MESSENGER-RNA CONTENT IN HYPOTHYROID RAT-LIVER
The effect of acetyl-L-carnitine on the quantity of the messenger RNA for the subunit I of cytochrome oxidase in the liver mitochondria of hypothyroid rat was measured by Northern blot and solution hybridization. Three hours after pre-treatment of hypothyroid rat with acetyl-L-carnitine, the level of the transcript increased strongly. This effect was also obtained when acetyl-L-carnitine was administered to T3 pre-treated hypothyroid rats. These results add further evidence to the suggestion that acetyl-L-carnitine is able to stimulate mitochondrial transcription under altered metabolic conditions
Acetyl-l-carnitine prevents alteration of mitochondrial biogenesis, mitochondrial dynamics and mitochondrial antioxidant defenses in the heart of old rat
Decrease of D-loop frequency in heart and cerebral hemispheres mitochondrial DNA of aged rat
A quantitative analysis of the frequency of the supercoiled mitochondrial DNA molecules containing the D-loop in rat heart and cerebral hemispheres, at different ages, is presented. Both tissues of aged animals exhibit a remarkable reduction in the content of supercoiled D-loop containing molecules compared to the adults. This alteration could be responsible for the age-dependent reduction of mitochondrial DNA transcription previously observed in rat brain and heart
LIPID-COMPOSITION IN SYNAPTIC AND NONSYNAPTIC MITOCHONDRIA FROM RAT BRAINS AND EFFECT OF AGING
The cholesterol, phospholipid, and fatty acid compositions in synaptic and nonsynaptic mitochondria from rat brains and the effect of aging were studied. Both cholesterol and phospholipid contents were found to be significantly different in synaptic compared to nonsynaptic mitochondria. In both types of brain mitochondria, aging decreases the cholesterol content by 27% and the phospholipid content by approximately 12%. The difference between these decreases observed in the organelles causes decreases in the cholesterol/phospholipid molar ratios for synaptic and nonsynaptic mitochondria of 17 and 19%, respectively. Also, the phospholipid composition is significantly different in synaptic compared to nonsynaptic mitochondria. Among phospholipids, only the cardiolipin fraction showed a significant decrease (26%) in nonsynaptic mitochondria from the brains of aged rats. Instead, the fatty acid composition was not significantly different in synaptic compared to nonsynaptic mitochondria. The 21% aging decrease in linoleic acid (18:2), observed only in nonsynaptic mitochondria, may be related to a decrease in cardiolipin, which contains a large amount of this fatty acid
Is acetyl-L-carnitine able to reduce oxidative stress in the liver of aging rat by favouring mitochondrial biogenesis?
Quantitation of mitochondrial RNA species during rat liver development: the concentration of cytochrome oxidase subunit I (COI) mRNA increases at birth
DmTTF, a novel mitochondrial transcription termination factor that recognises two sequences of Drosophila melanogaster mitochondrial DNA
Using a combination of bioinformatic and molecular biology approaches a Drosophila melanogaster
protein, DmTTF, has been identified, which exhibits sequence and structural similarity with two mitochondrial
transcription termination factors, mTERF (human) and mtDBP (sea urchin). Import/processing
assays indicate that DmTTF is synthesised as a precursor of 410 amino acids and is imported into
mitochondria, giving rise to a mature product of 366 residues. Band-shift and DNase I protection experiments
show that DmTTF binds two homologous, short, non-coding sequences of Drosophila mitochondrial
DNA, located at the 3' end of blocks of
genes transcribed on opposite strands. The location of the target sequences coincides with that of two of
the putative transcription termination sites previously hypothesised. These results indicate that DmTTF is the termination factor of mitochondrial
transcription in Drosophila. The existence of two DmTTF binding sites might serve not only to stop
transcription but also to control the overlapping of a large number of transcripts generated by the
peculiar transcription mechanism operating in this organism
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