[show abstract][hide abstract] ABSTRACT: Conditions for the realization in rats of moderate physiological stress (PHS) (30-120min) were selected, which preferentially increase adaptive restorative processes without adverse responses typical of harmful stress (HST). The succinate dehydrogenase (SDH) and α-ketoglutarate dehydrogenase (KDH) activity and the formation of reactive oxygen species (ROS) in mitochondria were measured in lymphocytes by the cytobiochemical method, which detects the regulation of mitochondria in the organism with high sensitivity. These mitochondrial markers undergo an initial 10-20-fold burst of activity followed by a decrease to a level exceeding the quiescent state 2-3-fold by 120min of PHS. By 30-60min, the rise in SDH activity was greater than in KDH activity, while the activity of KDH prevailed over that of SDH by 120min. The attenuation of SDH hyperactivity during PHS occurs by a mechanism other than oxaloacetate inhibition developed under HST. The dynamics of SDH and KDH activity corresponds to the known physiological replacement of adrenergic regulation by cholinergic during PHS, which is confirmed here by mitochondrial markers because their activity reflects these two types of nerve regulation, respectively. The domination of cholinergic regulation provides the overrestoration of expenditures for activity. In essence, this phenomenon corresponds to the training of the organism. It was first revealed in mitochondria after a single short-time stress episode. The burst of ROS formation was congruous with changes in SDH and KDH activity, as well as in ucp2 and cox3 expression, while the activity of SDH was inversely dependent on the expression of the gene of its catalytic subunit in the spleen. As the SDH activity enhanced, the expression of the succinate receptor decreased with subsequent dramatic rise when the activity was becoming lower. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaption and therapy.
The international journal of biochemistry & cell biology 07/2012; · 4.89 Impact Factor
[show abstract][hide abstract] ABSTRACT: We measured the activity of mitochondrial succinate dehydrogenase (SDH) within cells, in media with near-physiological composition, in lymphocytes immobilized in a blood smear on glass. SDH activity was studied in newborn rats characterized by natural hyperadrenergic status and also in adult animals injected with epinephrine. In most newborns very high activities were recorded, which exceeded the activities in adults at rest 7-8-fold or 3-fold according to the conventional calculation, or more than 30- and 6-fold according to our more precise calculation. The findings support our concept about a selective interaction between adrenergic stimulation and oxidation of succinic acid. According to this concept, epinephrine and norepinephrine specifically activate oxidation of succinic acid, whereas blood micromolar concentrations of the latter stimulate the release of catecholamines (the receptor-mediated signaling effect). This interaction is half of a substrate-hormonal regulatory system responsible for connection of vegetative nervous system with oxidation in mitochondria of the innervated organs. The increase in succinate oxidation by catecholamines includes activation of the faster pathways of succinate generation than the complete Krebs cycle, in particular, the glyoxylate cycle that is shown in the newborn rats in the present study.
[show abstract][hide abstract] ABSTRACT: Respiration parameters of liver mitochondria (MCh) in rats fed with amaranth seed oil for 3 weeks have been evaluated. Thirty
minutes before decapitation, adrenaline was injected intraperitoneally at a low dose (350 μg/kg body weight) to both control
and experimental animals. It was shown that in animals that were injected with adrenaline and did not receive oil, the rate
of phosphorylating respiration increased by 32% and phosphorylation time decreased by 22% upon oxidation of succinate; upon
oxidation of α-ketoglutarate in the presence of the succinate dehydrogenase inhibitor malonate, phosphorylating respiration
was activated by 23%. The respiration of MCh upon oxidation of succinate + glutamate and α-ketoglutarate in the absence of
malonate was not affected by adrenaline. The intake of oil markedly activated almost all parameters of mitochondrial respiration
in experimental rats upon oxidation of all above-listed substrates in both coupled and uncoupled MCh. However, phosphorylation
time was close to the control value (upon oxidation of succinate) or increased (upon oxidation of α-ketoglutarate in the presence
and absence of malonate). The injection of adrenaline to animals receiving oil did not affect the oil-activated respiration
of MCh oxidizing the substrates used; however, phosphorylation time in all groups of animals decreased. Ca2+ capacity of MCh in rats receiving amaranth oil did not change. Thus, our data show that feeding of rats with amaranth oil
activates mitochondrial respiration and prevents MCh hyperactivation induced by adrenaline.
Biochemistry (Moscow) Supplement Series A Membrane and Cell Biology 02/2008; 2(1):40-47.
[show abstract][hide abstract] ABSTRACT: The role of impairment of general oxidative and energy metabolism in pathogenesis of lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH) and their correction by (1-adrenoblocker alfuzosin was studied. One group of patients (N = 126) was examined by standard methods for determination of the severity of LUTS by IPSS and mean effective volume of urinary bladder (MEVUB). In the second group (N = 29) in addition to functional examinations, metabolic indicators in blood were measured: antioxidant activity (AOA) and succinate dehydrogenase activity (SDA). Severity of LUTS depends greatly on the MEVUB. It was the first to show a practically complete correlation between LUTS, AOA and SDA. Severity of LUTS exactly correlates with indicators of oxidative and energy metabolism. In patients with more heavy LUTS, lowest AOA and SDA values were found. In the course of effective treatment, both phenomena developed an improvement of clinical symptoms and a rise of biochemical parameters. Close correlation between functional and metabolic phenomena is evidence of an essential role of metabolic mechanisms in the pathogenesis of LUTS with BPH. This opens perspectives to use antioxidants and energy metabolism activators for correction of UB dysfunction in patients with BPH.
[show abstract][hide abstract] ABSTRACT: Using an original cytobiochemical method to study oxidation in mitochondria, preserving their native network organization within cells in a blood smear, we have revealed a hyperactive state of succinate dehydrogenase that arises in the organism under physiological stress. This is generally consistent with the notion of non-equilibrium state of enzymes during their activity. The mechanism moderating the succinate dehydrogenase hyperactivity is based on full-fledged functioning of α-ketoglutarate dehydrogenase, sup-ported by oxidation of isocitrate.