Fwd: [CasiClubhouse] mitochondria terminology: disease disorder dysfunction

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The new "1 in 200" findings are important. The review by Rossignol and

Bradstree presents important distinctions between classic mitochondria

disease and a more widespread mitochondria dysfunction (0). As we've

seen, vaccinology's establishmentarians are inclined to establish in

the public mind that mito disease is a very rare occurrence. Herein are

some google search strategies and 5 citations free online, perhaps

useful in countering myths likely to be perpetrated by

vaccination-business zealots.

- - - -

Mitochondrial google wallowings:

"mitochondria disease" definition

"mitochondria disorder" definition

"mitochondria dysfunction" definition

0. Evidence of Mitochondrial Dysfunction in Autism and Implications

for Treatment

A. Rossignol and J. Bradstreet

Am J of Biochem Biotech 4(2): 208-217 , 2008

http://www.scipub.org/fulltext/ajbb/ajbb42208-217.pdf

Classical mitochondrial diseases occur in a subset of individuals with

autism and are usually caused by genetic anomalies or mitochondrial

respiratory pathway deficits. However, in many cases of autism, there

is evidence of mitochondrial dysfunction (MtD) without the classic

features associated with mitochondrial disease. MtD appears to be more

common in autism and presents with less severe signs and symptoms. It

is not associated with discernable mitochondrial pathology in muscle

biopsy specimens despite objective evidence of lowered mitochondrial

functioning. Exposure to environ-mental toxins is the likely etiology

for MtD in autism. This dysfunction then contributes to a number of

diagnostic symptoms and comorbidities observed in autism including:

cognitive impairment, language deficits, abnormal energy metabolism,

chronic gastrointestinal problems, abnormalities in fatty acid

oxidation, and increased oxidative stress. MtD and oxidative stress may

also explain the high male to female ratio found in autism due to

increased male vulnerability to these dysfunctions. Biomarkers for

mitochondrial dysfunction have been identified, but seem widely

under-utilized despite available therapeutic interventions. Nutritional

supplementation to decrease oxidative stress along with factors to

improve reduced glutathione, as well as hyperbaric oxygen therapy

(HBOT) represent supported and rationale approaches. The underlying

pathophysiology and autistic symptoms of affected individuals would be

expected to either improve or cease worsening once effective treatment

for MtD is implemented.

1: Br J

Pharmacol. 2007 Aug;151(8):1154-65. Epub 2007 May 21.

Related

Articles,

Links

Mitochondrial medicine: pharmacological

targeting of mitochondria in disease.

Armstrong

JS.

Department of Biochemistry, Faculty of Medicine, National University of

Singapore, 8 Medical Drive, Singapore 117597, Singapore.

Mitochondria

play a central role in cell life and death and are known to be

important in a wide range of diseases including the cancer, diabetes,

cardiovascular disease, and the age-related neurodegenerative diseases.

The unique structural and functional characteristics of mitochondria

enable the selective targeting of drugs designed to modulate the

function of this organelle for therapeutic gain. This review discusses

mitochondrial drug targeting strategies and a variety of novel

mitochondrial drug targets including the electron transport chain,

mitochondrial permeability transition, Bcl-2 family proteins and

mitochondrial DNA. Mitochondrial drug-targeting strategies will open up

avenues for manipulating mitochondrial functions and allow for

selective protection or eradication of cells for therapeutic gain in a

variety of diseases.

Publication Types:

Review

PMID: 17519949 [PubMed - indexed for MEDLINE]

PMCID: PMC2189819

2: Circ Res.

2007 Apr 27;100(8):1128-41.

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Articles,

Links

Endothelial mitochondria: contributing to

vascular function and disease.

son

SM, Duchen

MR.

The

Hatter Cardiovascular Institute, Department of Medicine, Royal Free and

University College Medical School, London, United Kingdom.

s.davidson@...

Disturbances in vascular function

contribute to the development of several diseases of increasing

prevalence and thereby contribute significantly to human mortality and

morbidity. Atherosclerosis, diabetes, heart failure, and ischemia with

attendant reperfusion injury share many of the same risk factors, among

the most important being oxidative stress and alterations in the blood

concentrations of compounds that influence oxidative stress, such as

oxidized low-density lipoprotein. In this review, we focus on

endothelial cells: cells in the frontline against these disturbances.

Because ATP supplies in endothelial cells are relatively independent of

mitochondrial oxidative pathways, the mitochondria of endothelial cells

have been somewhat neglected. However, they are emerging as agents with

diverse roles in modulating the dynamics of intracellular calcium and

the generation of reactive oxygen species and nitric oxide. The

mitochondria may also constitute critical "targets" of oxidative

stress, because survival of endothelial cells can be compromised by

opening of the mitochondrial permeability transition pore or by

mitochondrial pathways of apoptosis. In addition, evidence suggests

that endothelial mitochondria may play a "reconnaissance" role. For

example, although the exact mechanism remains obscure, endothelial

mitochondria may sense levels of oxygen in the blood and relay this

information to cardiac myocytes as well as modulating the vasodilatory

response mediated by endothelial nitric oxide.

Publication Types:

Research

Support, Non-U.S. Gov't

Review

PMID: 17463328 [PubMed - indexed for MEDLINE]

3: Diabetes.

2004 Feb;53 Suppl 1:S96-102.

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Articles,

Links

Roles of mitochondria in health and disease.

Duchen

MR.

Department of Physiology, University College London, London, UK.

m.duchen@...

Mitochondria

play a central role in cell life and cell death. An increasing number

of studies place mitochondrial dysfunction at the heart of disease,

most notably in the heart and the central nervous system. In this

article, I review some of the key features of mitochondrial biology and

focus on the pathways of mitochondrial calcium accumulation.

Substantial evidence now suggests that the accumulation of calcium into

mitochondria may play a key role as a trigger to mitochondrial

pathology, especially when that calcium uptake is accompanied by

another stressor, in particular nitrosative or oxidative stress. The

major process involved is the opening of the mitochondrial permeability

transition pore, a large conductance pore that causes a collapse of the

mitochondrial membrane potential, leading to ATP depletion and necrotic

cell death or to cytochrome c release and apoptosis, depending on the

rate of ATP consumption. I discuss two models in particular in which

these processes have been characterized. The first is a model of

oxidative stress in cardiomyocytes, in which reperfusion after ischemia

causes mitochondrial calcium overload, and oxidative stress. Recent

experiments suggest that cardioprotection by hypoxic preconditioning or

exposure to the ATP-dependent K(+) channel opener diazoxide increases

mitochondrial resistance to oxidative injury. In a second model, of

calcium overload in neurons, the neurotoxicity of glutamate depends on

mitochondrial calcium uptake, but the toxicity to mitochondria also

requires the generation of nitric oxide. Glutamate toxicity after

activation of N-methyl-D-aspartate (NMDA) receptors results from the

colocalization of NMDA receptors with neuronal nitric oxide synthase

(nNOS). The calcium increase mediated by NMDA receptor activation is

thus associated with nitric oxide generation, and the combination leads

to the collapse of mitochondrial membrane potential followed by cell

death.

Publication Types:

Research

Support, Non-U.S. Gov't

Review

PMID: 14749273 [PubMed - indexed for MEDLINE]

4: J

Biomed Biotechnol. 2003;2003(3):162-163.

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Articles,

Links

Hypoperfusion, Mitochondria Failure, Oxidative

Stress, and Alzheimer Disease.

Aliev

G, Obrenovich

ME,

MA,

G.

PMID: 12975531