Male infertility is one of the most stressful factors of couples, being present in about 40% cases.It is usually caused by a low number of sperm (oligozoospermia) or poor sperm motility (asthenozoospermia).The sperm motility is used as an indicator of semen quality and male infertility.To the impairment of male reproduction health can contribute genetic, nutritional and environmental factors, smoking and drugs.It is well documented that excessive reactive oxygen species (ROS) production decreases sperm motility, impairs sperm function, damages the morphology of spermatozoa (1, 2).To the decreased sperm motility contribute also disturbances of sperm mitochondrial function and energy production, low levels of coenzyme Q 10 and carnitine, as well as sperm mitochondrial deoxyribonucleic acid (DNA) defects.The origin of sperm dysfunction, however, is not well understood.Background: Oxidative stress has been established as a major factor in the pathogenesis of male infertility.Low level of coenzyme Q 10 contributes to the decreased sperm motility, which plays a vital role in sperm mitochondrial energy production and neutralization of reactive oxygen species (ROS).The aim of the present study was to fi nd out, if an assessment of coenzyme Q 10-TOTAL (CoQ 10-TOTAL ), α-tocopherol, γ-tocopherol and oxidative stress could contribute to the diagnosis of infertility in men.Subjects and methods: Two groups of infertile men, according to sperm motility (a+b and b+c) were included in the study.CoQ 10-TOTAL , α-tocopherol, γ-tocopherol in plasma and seminal fl uid, and parameter of oxidative stress (thiobarbituric acid reactive substances -TBARS) in plasma were determined.Results: Higher sperm density and decreased sperm pathology were found in group a+b vs b+c (class a and bfast and weak forward motility, class c -nonprogressive motility).Concentrations of CoQ 10-TOTAL and α-tocopherol were signifi cantly increased in seminal fl uid of groups a+b vs b+c, opposite results were estimated in plasma.Concentrations of γ-tocopherol in plasma and seminal fl uid of both groups were similar.Plasmatic TBARS concentrations were increased in both groups of infertile men. Conclusion:We suppose that incorporation of oxidative stress assessment, CoQ 10-TOTAL and α-tocopherol concentrations in seminal fl uid and plasma into routine andrology can play an important role for the diagnosis and targeted therapy of male infertility (Tab. 1, Ref. 16).
Concentrations ranging from 1-9 x 10(-7) mol.dm-3 were employed for in vitro studies. Under the selected experimental conditions, both agents markedly decreased the stimulated consumption of oxygen by the cardiac muscle mitochondria in the condition S3, the rate of the formation of energy by mitochondria as well as the respiratory control index. The coefficient of oxidative phosphorylation was not markedly changed due to the effect of the added agents. The results of the present paper suggest possible integration of the cardiac muscle mitochondria in the oxidative metabolism of the potential beta-adrenolytic agents FA33 and FP33, which requires further in vivo studies.
Purpose: Mitochondria (MIT) from hearts of rats with acute streptozotocin (STZ)-diabetes (DIA) and hearts subjected to remote preconditioning induced by limb ischemia (R-PC) exhibited functional remodeling of membranes followed by a cascade of changes reflecting a dynamic equilibrium between the pathological processes and the processes of endogenous protection (EP). Aim of the study was to investigate the effects of R-PC and PC - induced acute diabetes mellitus (DM), on the biophysical and biochemical properties of cardiac MIT.
Methods: Male Wistar rats (220±20g) were used in the experiment. DIA was induced by a single dose of STZ, (65 mg/kg, i.p.). R-PC was induced by 3 series of 5 min. ischemia and 5 min. reperfusion. Hearts were rapidly excised, perfused in the Langendorff mode and exposed to 30 min. global ischemia and 40 min reperfusion. MIT were isolated by means of differential centrifugation combined with protease treatment. Mg2+-dependent and 2, 4-dinitrophenol - stimulated ATPase activity was determined by estimation of Pi liberated from ATP splitting. Membrane fluidity (MF) of isolated MIT was assessed by measuring fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene. Content of oxidized isoforms of the coenzyme Q (CoQ9-ox and CoQ10-ox) in the MIT was assessed by means of HPLC and the content of conjugate dienes (CD) was determined spectrophotometrically at 230 nm.
Results: MIT from acute (8 days) DIA hearts exhibited significantly (p<0.05) elevated MF and Mg2+-ATPase activities. An increase in MF was also observed in R-PC and it remained present even after ischemia and post-ischemic reperfusion. Free radicals created in heart MIT in the time course of development of the DIA left the MIT membrane without inducing any considerable increase in the amount of CD or decrease in fluidity of the lipid bilayer. On the other hand, the increase in oxidized formes of the CoQ9-ox and CoQ10-ox in the MIT membrane occurred in sense of the old paradigm that radicals-induced oxidative changes in components of the respiratory chain are at least co-responsible for its malfunction in diabetes.
Conclusions: Our findings confirmed that the changes in properties and function of MIT membranes associated with DIA- and R-PC-induced remodeling are intimately involved in increased ischemia-tolerance of the myocardium. Grants: VEGA 2/0101/12, APVV 0102-11, KEGA 003 UK-4/2012.
The effect of inhalation of cigarette smoke (passive smoking) on the oxidative and phosphorylating processes of rabbit myocardial mitochondria was studied in three experimental models after a single smoke lasting 30 min, after 2 weeks smoking twice daily and after 8 weeks smoking twice daily. A significant decrease in respiration as well as in the phosphorylation rate of mitochondria was found; whereas the respiratory control index and coefficient of oxidative phosphorylation did not change. Both factors of cigarette smoke (carbon monoxide and nicotine) participate in the metabolic injury of mitochondria. Long term cigarette smoking causes considerable metabolic and morphological alterations to the heart muscle which can be characterised as smoke cardiomyopathy.
