Studies of the human aortic intima by a direct quantitative assay of mutant alleles in the mitochondrial genome.

A mutant allele quantitative assay was developed to study somatic mitochondrial mutations associated with human diseases. This assay may be used in the clinical diagnostics for diseases associated with somatic mutations. To detect somatic mutations associated with atherosclerotic lesions of the aortal intima, we analyzed 40 mitochondrial mutations previously identified in several pathological conditions.

[Mitochondrial energy conversion disturbance with decrease in ATP production as a source of systemic arterial hypertension].

This review deals with the cellular mechanisms underlying decreased energy status documented in different tissues from experimental rat models of primary and secondary hypertension as well as the involvement of these abnormalities in the pathogenesis of the disease. Such analyses allow us to hypothesize that dysfunction of mitochondrial energy conversion, caused by distinct stimuli, including generalized disturbances of intracellular Ca2+ handling and mitochondria calcium overload found in primary hypertension, leads to uncoupling of oxidation and phosphorylation and attenuated ATP synthesis. Examples of arterial hypertension accompanied by mitochondrial uncoupling and cell ATP depletion (hyperthyroidism, cold hypertension, cyclosporine A intake, etc.

[Calcium induced calcium release from liver mitochondria of spontaneously hypertensive rats].

Background: Disturbances of ionic homeostasis of cells and recently discovered cellular energy deficiency due to reduced ATP-synthesizing ability of mitochondria are the most important components of pathogenesis of primary hypertension. Therefore it is essential to elucidate relationship between functioning of ionic transport systems especially that of calcium transport and ATP-synthesizing ability of mitochondria.

Aim: To study calcium induced calcium release from liver mitochondria of spontaneously hypertensive rats at various initial calcium concentrations in medium.

[Decreased ATP-synthesis ability of brain mitochondria in spontaneously hypertensive rats].

Unlabelled: It has been shown previously that a decrease of ATP amount and changed balance of other macroergic phosphates occurs in different tissues of spontaneously hypertensive rats (SHR) compared with control normotensive rats (WKY).

Aim: To assess the ability of SHR brain isolated mitochondria to synthesize ATP and to elucidate its relation to extramitochondrial calcium concentration.

Results: The present work shows for the first time that SHR brain mitochondria initially differ from WKY ones by decreased (by 30%) ATP synthesis rate.

[Decreased ATP-synthesis ability of liver mitochondria in spontaneously hypertensive rats (SHR): role of calcium overload of the mitochondria].

It has been shown previously, that a decrease of ATP amount and changed balance of the other macroergic phosphates are observed in different tissues of spontaneously hypertensive rats (SHR) compared with the normotensive controls (WKY). The aim of the present study was to assess the ability of SHR liver isolated mitochondria to synthesize ATP and to clarify its dependence on extramitochondrial calcium concentration. Macroergic phosphate concentrations were measured by high performance liquid chromatography (HPLC).