Fish occurrence in the middle Volga and upper Don regions (Russia).

Background: In ichthyological publications from both Russia as a whole, and from the study region, lack of data indicating the actual results of observations in a specific place all result in publication of a generalised analysis. Although our publications contain such data, they are, however, not convenient for users performing global analysis. The main purpose of publishing a database is to make our data available in the global biodiversity system to a wide range of users.

Lipid peroxidation and antioxidant enzyme activity in aspirin-treated rats.

1. Malondialdehyde formation and antioxidant enzyme activity after oral or intraperitoneal treatment of rats with various doses of aspirin was studied. 2.

In vitro effects of aspirin on malondialdehyde formation and on activity of antioxidant and some metal-containing enzymes.

The in vitro effects of aspirin in different concentrations on malondialdehyde formation and on the activity of antioxidant and some metal-containing enzymes in rat liver homogenate and erythrocytes were studied. Aspirin showed a biphasic dependence on concentration: low concentrations (to 1.0 mM) stimulated the spontaneously formed malondialdehyde in the liver homogenate and the high concentration (5.

Lipid peroxidation and antioxidant enzymes in vanadate-treated rats.

Male Wistar rats received an aqueous solution of ammonium metavanadate (AMV) of 0.15 mg/V/ml concentration instead of water for 14 days. The erythrocyte count and haemoglobin level in blood were not changed; the haematocrit index was slightly increased.

Vanadyl causes hydroxyl radical mediated degradation of deoxyribose.

Vanadyl caused a time- and dose-dependent degradation of deoxyribose to carbonyl products detectable with thiobarbituric acid. This process was inhibited by catalase, ethanol or HEPES; whereas superoxide dismutase was without effect. Vanadate did not substitute for vanadyl even in the presence of a source of O2- plus H2O2; but it did so in the presence of reductants such as thiols or NADH.

Effects of vanadate on the oxidation of NADH by xanthine oxidase.

Vanadate (V(V)) stimulates the oxidation of NADH by xanthine oxidase and superoxide dismutase eliminates the effect of V(V). Paraquat stimulates both the oxidation of NADH by xanthine oxidase and the V(V) enhancement of that oxidation. Xanthine, which is a better substrate for xanthine oxidase than is NADH, causes a V(V)-dependent co-oxidation of NADH which is transient and eliminated by SOD.

Phosphatidylcholine peroxidation induced by Cu(II) and some Cu(II) complexes.

We established that Cu(II) and its complexes with aspirin, indomethacin and cimetidine produced lipid peroxidation in phosphatidylcholine suspension. Ionic copper was found to have the most pronounced effect, while the effect of the complexes depends on the ligand. Neither of the ligands exerted a prooxidative effect.

A study on the mechanism of the vanadate-dependent NADH oxidation.

The mechanism of the vanadate (V(V]-dependent oxidation of NADH was different in phosphate buffers and in phosphate-free media. In phosphate-free media (aqueous medium or HEPES buffer) the vanadyl (V(IV] generated by the direct V(V)-dependent oxidation of NADH formed a complex with V(V). In phosphate buffers V(IV) autoxidized instead of forming a complex with V(V).

Vanadyl- and vanadate-induced lipid peroxidation in mitochondria and in phosphatidylcholine suspensions.

Vanadyl (V(IV] was found to induce rapidly developing lipid peroxidation in intact and sonicated mitochondria as well as in phosphatidylcholine suspension. The ability of vanadate (V(V] to induce lipid peroxidation was much less pronounced compared to that of vanadyl. The peroxidative action of vanadate on phosphatidylcholine much increased in the presence of NADH and ascorbate.

The hemolytic effect of copper complexes with different ligands.

The effect of Cu(II) and Cu(II) complexes/Cu(II)(cimetidine)2 Cu(II)(glycine) and Cu(II)(glycine)2/on the rat and human erythrocytes was studied. Time- and dose-dependence of the Cu(II) complexes-induced hemolysis, oxidation of hemoglobin and formation of precipitates of denaturated hemoglobin were established. The hemolytic effect of Cu(II)complexes was abolished by strong complexons of Cu(II) and by physiological concentrations of albumin and histidine.

The effects of aspirin, indomethacin and their copper complexes on phospholipase activity and on lipid peroxidation in rat liver microsomes.

Aspirin and indomethacin decreased the hydrolysis of microsomal phospholipids by exogenous soluble phospholipase A2 and increased lipid peroxidation in rat liver microsomes. Copper chelates of the non-steroidal anti-inflammatory drugs tested more strongly decreased the activity of soluble phospholipase A2 as compared to the ligands. In contrast to the stimulant effects of aspirin and indomethacin these chelates exerted dose-dependent inhibitory effects on enzymatic and non-enzymatic lipid peroxidation.

In vitro study of paraquat effects on malondialdehyde formation in thymus cells.

The present experiments have shown that paraquat enhanced both O2- production and oxidation of exogenous NADPH in thymus cells by NADPH-dependent enzyme system. The effects of paraquat on malondialdehyde formation were also NADPH-dependent and opposite in the absence and in the presence of ferrous ions: Paraquat inhibited the NADPH-dependent malondialdehyde formation in the absence of Fe2+; it activated this formation in the presence of Fe2+ and had no effect on the nonenzymic Fe2+- and Fe2+-ascorbate-stimulated lipid peroxidation. It is suggested that the activating effect of paraquat on the enzymic NADPH-dependent MDA formation in the presence of Fe2+ is due to the formation of a powerful oxidant product (FeO2)+ or to some Fe2+-paraquat radical complex, acting similarly to the ADP-chelated ferrous ions.

Lipid peroxidation in liver mitochondria from copper-loaded rats.

The amount of phospholipids in liver mitochondria decreased after chronic alimentary copper-loading of rats (40 mg CuSO4 per rat per day in the course of two weeks), while 24 hours after a single intraperitoneal injection of copper (20 mg CuSO4 per kg body weight) it remained unchanged, notwithstanding that both copper treatments highly increased the copper level in mitochondria. Alimentary copper-loading led to a decrease in the relative proportions of the majority of unsaturated fatty acids in mitochondrial phospholipids. Both the spontaneous and Fe2+-induced formation of malonaldehyde were more enhanced in the mitochondria from the two experimental groups as compared to the controls.

Reduction of Cu2+ by isolated rat liver mitochondria.

The present work provided evidence that isolated rat liver mitochondria reduce the larger part of the added CU2+ and that the reduction is of important for copper accumulation in mitochondria. The process is rapid, energy-independent and affected by steric factors. Both mitochondrial thiols and cytochrome c could participate in the Cu2+-reduction.

Ascorbate and Fe++-induced lipid peroxidation in liver mitochondria isolated from copper-deficient rats.

The effects of ascorbate and Fe++ on lipid peroxidation are compared in liver mitochondria isolated from control and copper-deficient rats. Spontaneous, Fe++- and ascorbate-induced formation of compounds reacting with the thiobarbituric acid (TBA) and the swelling in the mitochondria are studied as indicators of lipid peroxidation. The initial level of TBA-reacting compounds in freshly isolated copper-deficient mitochondria is higher than that in the control mitochonidria.

Cu2+-effects on mitochondrial resistance to sodium deoxycholate.

The effect of the preincubation of mitochondria with different doses of Cu2+ on the action of sodium deoxycholate (DOC) was studied. The amount of protein released from mitochondria upon their treatment with Cu2+ as an indice for the intactness of mitochondria was studied, too. On the account of Cu2+-influence on the level of mitochondrial SH groups Cu2+-effects on the action of DOC were compared with those of a thiol reagent p-chlormercuribenzoate (p-CMB).

Effect of crataemon on the respiration of isolated mitochondria.

Crataemon is a drug containing the total mixture of flavonoids isolated from the leaves of Crataegus minogina. Crataemon causes activation and inhibition of the respiration of isolated liver and heart mitochondria, with different time and dose dependence and with different sensitivity to EDTA. The activating effect develops immediately, it is caused by small doses of crataemon, it is lacking in uncoupled mitochondria and completely abolished by EDTA.