X Julien
Mitochondrial energy metabolism and ageing.
Bratic I, Trifunovic A.
Cologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated
Diseases (CECAD), University of Cologne, D-50674 Cologne, Germany; Division of
Metabolic Diseases, Department of Laboratory Medicine, Karolinska Institutet,
S-14186 Stockholm, Sweden.
Ageing can be defined as a progressive, generalized impairment of function,
resulting in an increased vulnerability to environmental challenge and a growing
risk of disease and death. Ageing is likely a multifactorial process caused by
accumulated damage to a variety of cellular components. During the last 20years,
gerontological studies have revealed different molecular pathways involved in the
ageing process and pointed out mitochondria as one of the key regulator of
longevity. Increasing age in mammals correlates with increased levels of
mitochondrial DNA (mtDNA) mutations and a deteriorating respiratory chain
function. Experimental evidence in the mouse has linked increased levels of
somatic mtDNA mutations to a variety of ageing phenotypes, such as osteoporosis,
hair loss, graying of the hair, weight reduction and decreased fertility. A
mosaic respiratory chain deficiency in a subset of cells in various tissues, such
as heart, skeletal muscle, colonic crypts and neurons, is typically found in aged
humans. It has been known for a long time that respiratory-chain-deficient cells
are more prone to undergo apoptosis and an increased cell loss is therefore
likely of importance in the age-associated mitochondrial dysfunction. In this
review, we would like to point out the link between the mitochondrial energy
balance and ageing, as well as a possible connection between the mitochondrial
metabolism and molecular pathways important for the lifespan extension. Copyright
© 2009. Published by Elsevier B.V.
PMID: 20064485 [PubMed - as supplied by publisher]
Soluzione?
Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic
approach with fucoidan.
Veena CK, Josephine A, Preetha SP, Rajesh NG, Varalakshmi P.
Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic
Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113,
India.
Oxalate/calcium oxalate toxicity is mediated through generation of reactive
oxygen species in a process that partly depends upon events that induce
mitochondrial damage. Mitochondrial dysfunction is an important event favoring
stone formation. The objective of the present study was to investigate whether
mitochondria is a target for oxalate/calcium oxalate and the plausible role of
naturally occurring glycosaminoglycans from edible seaweed, fucoidan in
ameliorating mitochondrial damage. Male albino rats of Wistar strain were divided
into four groups and treated as follows: Group I: vehicle treated control, Group
II: hyperoxaluria was induced with 0.75% ethylene glycol in drinking water for 28
days, Group III: fucoidan from F. vesiculosus (5 mg/kg b.wt, s.c) from the 8th
day of the experimental period, Group IV: ethylene glycol+fucoidan treated rats.
The tricarboxylic acid (TCA) cycle enzymes like succinate dehydrogenase,
isocitrate dehydrogenase, malate dehydrogenase and respiratory complex enzyme
activities were assessed to evaluate mitochondrial function. Oxidative stress was
assessed based on the activities of antioxidant enzymes, level of reactive oxygen
species, lipid peroxidation and reduced glutathione. Mitochondrial swelling was
also analyzed. Ultra structural changes in renal tissue were analyzed with
electron microscope. Hyperoxaluria induced a decrease in the activities of TCA
cycle enzymes and respiratory complex enzymes. The oxidative stress was evident
by the decrease in antioxidant enzymes, glutathione and an increase in reactive
species and lipid peroxidation in mitochondria. Mitochondrial damage was evident
by increased mitochondrial swelling. Administration of fucoidan, decreased
reactive oxygen species, lipid peroxidation (P<0.05), mitochondrial swelling and
increased the activities of antioxidant enzymes and glutathione levels (P<0.05)
and normalized the activities of mitochondrial TCA cycle and respiratory complex
enzymes (P<0.05). From the present study, it can be concluded that mitochondrial
damage is an essential event in hyperoxaluria, and fucoidan was able to
effectively prevent it and thereby the renal damage in hyperoxaluria.
PMID: 18001705 [PubMed - indexed for MEDLINE]
Mitochondrial damage, cytotoxicity and apoptosis in iron-potentiated alcoholic
liver fibrosis: amelioration by taurine.
Lakshmi Devi S, Anuradha CV.
Department of Biochemistry and Biotechnology, Annamalai University, Annamalai
Nagar, Chidambaram, 608 002, Tamil Nadu, India.
Taurine effectively prevents ischemia-induced apoptosis in the cardiomyocytes and
hypothalamic nuclei. The present study explores the influence of taurine on
mitochondrial damage, oxidative stress and apoptosis in experimental liver
fibrosis. Male albino Wistar rats were divided into six groups and maintained for
a period of 60 days as follows: Group I, control; Group II, ethanol treatment [6
g/(kg/day)]; Group III, fibrosis induced by ethanol and iron (0.5% w/w); Group
IV, ethanol + iron + taurine (2% w/v); Group V, ethanol + taurine treatment and
Group VI, control + taurine treatment. Hepatocytes isolated from ethanol plus
iron-treated rats showed decreased cell viability and redox ratio, increased
reactive oxygen species formation, lipid peroxidation, DNA fragmentation, and
formation of apoptotic bodies. Liver mitochondria showed increased susceptibility
to swell, diminished activities of mitochondrial respiratory chain complexes and
antioxidants. Taurine administration to fibrotic rats restored mitochondrial
function, reduced reactive oxygen species formation, prevented DNA damage, and
apoptosis. Thus taurine might contribute to the amelioration of the disease
process.
PMID: 19381777 [PubMed - as supplied by publisher]
Un integratore di kelp (titolato in fucoidani) e taurina sarebbe economico e, sulla carta, con ottime referenze. Che ne dici?
