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Antioxidant effect of paraaminobenzoic acid (PABA) in the retina upon different routes of its administration has been revealed previously. In this study we investigated the antioxidant effect of PABA in the cornea and lens of rats after its parabulbar injection. Antioxidant activity of PABA was compared to that of emoxipin. One hour after hypoxic hypoxia the animals were parabulbarly injected with PABA solutions (0.007-0.08%) and 1% emoxipin. The eyes of intact animals and rats exposed to hypoxia alone served as the control. The levels of lipid peroxidation products (hydroperoxide, malonic dialdehyde) and catalase activity in the cornea and lens were measured 1, 3, 6, and 11 h after injections. PABA in all studied concentrations essentially decreased the elevated levels of hydroperoxides and malonic dialdehyde and normalized catalase activity. The level of lipid peroxidation products and catalase activity normalized 24-28 h after hypoxia, while after PABA it normalized within 2-11 h. Antioxidant activity of emoxipin in the lens and cornea was the same as that of optimal antioxidant concentrations of PABA (0.02% for the cornea and 0.06% for the lens). Hence, PABA in a wide range of concentrations (0.007-0.06%) is characterized by sufficiently high antioxidant activity in tissues of the anterior segment of the eye (cornea and lens) upon local administration.

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Effect of Hirudo therapy on the activities of transport adenosine triphosphatases (ATPases) of the retina and pigmented epithelium (PE) is studied in normal and albino rabbits whose eyes were exposed to potent illumination (100,000 Lux at the level of the cornea for 90 min). The exposure decreased the activities of ATPase, which did not recover in any of animal groups. Hirudo therapy immediately after illumination increased the enzymes activity in pigmented animals in comparison with intact control: by 20% in the retina and by 23% in PE; Mg-ATPase activity increased by 23% in the retina and decreased by 10% in PE. In subsequent 24 h, ATPase activities decreased, but in comparison with exposed retina the activity of Na,K-ATPase in the retina was 70% increased and in PE 78% increased; the activities of Mg-ATPase were increased by 33 and 8%, respectively. Complete recovery of ATPase activities was attained in 8 days. In albino animals, ATPase activities did not recover completely, but they were notably higher than in intact controls. Hirudo therapy before illumination had a marked protective effect.

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Effect of Hirudo therapy on the level of lipid peroxidation (LPO) products and catalase activity in the retina and pigmented epithelium (PE) after exposure to intensive illumination is assessed. Light injury to the eye (100,000 lux in 90 min) leads to accumulation of LPO products and suppression of catalase activity. Hirudo therapy after potent light exposure of the eye decreased the level of hydroperoxide and malonic dialdehyde and normalized retinal and PE catalase activity, thus exerting a therapeutic antioxidant effect. Hirudo therapy before illumination did not notably protect the eye as regards the content of LPO products and catalase activity.

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Effect of para-aminobenzoic acid (PABA) on lipid peroxidation (LPO) in rat and guinea pig retina exposed to hypoxic hypoxia is studied. PABA was injected intraperitoneally and parabulbarly before and after hypoxic exposure. Antioxidant activities of PABA and emoxipin were compared. An intraperitoneal injection of PABA in a dose of 10 mg/kg 24 h before hypoxia virtually completely prevented accumulation of lipid peroxides and preserved catalase activity in the retina. Parabulbar injection of 0.01% PABA solution 1 h before hypoxia prevented LPO intensification, stabilized catalase activity in hypoxia, and protected the retina starting from the moment immediately after hypoxic exposure. The efficacy of 0.01% PABA is comparable with that of 1% emoxipin, and a 0.01% solution of emoxipin is less effective than PABA in the same concentration. PABA exerts an antioxidant effect after hypoxia by decreasing the abnormally high level of lipid peroxides and reducing catalase activity in the retina after parabulbar injection of the drug. All the studied concentrations of the drug (from 0.007 to 0.08%) are active, but the optimal dose for the retina is 0.04%. By its efficacy this concentration is equivalent to 1% emoxipin.

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The role of lipid peroxidation (LPO) in the lens capsule in its preservation under different conditions is investigated. The content of LPO products (hydroperoxides and malonic dialdehyde) appreciably increased in the lens capsule after preservation in normal and Ringer's saline for 1 to 6 days at 4 degrees C. These changes were paralleled by a reliable decrease in the content of various SH groups (Superficial, structurally masked protein, and glutathion) and in catalase activity. Preservation of the lens capsule in 1% gentamicin solution almost completely prevented such changes during the first 6 days of storage. Moreover, in model systems gentamicin suppressed the intensity of Fe(2+)-ascorbate-stimulated LPO. Intensification of LPO is believed to play an appreciable role in the structural and functional disorders in the lens capsule during its storage in different media. High antioxidative activity of gentamicin recommends it as an effective preserving agent for clinical purposes.

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Retinal response to the acute hypoxia and reoxygenation were shown to be independent of melanin presence in the eye pigmental epithelium (PE), i.e. in the retinas of both pigmented animals and albinos hypoxia survived an increase in the content of hydroperoxidases and malonyl dialdehyde; subsequent reoxygenation resulted in a more considerable accumulation of lipid peroxidation (LPO) products in both retinal types. Nevertheless under reoxygenation the number of malonyl dealdehyde became below the norm in PE of melanin-containing animals, but not in the albinos. At the same time acute hypoxia increased by 31% the electron spin resonance (ESR) uptake in the pigmented animals. Subsequent reoxygenation inconsiderably suppressed the intensity of the ESR signal. Under the above conditions pretreatment with Na2SeO3 increased the intensity of PE ESR uptake more than 2.5 times with following retrieval to the control level at the 20th minute of reoxygenation. We suggest that under hypoxia with subsequent reoxygenation the melano-protein granules favour regulation of LPO in PE, but not in other retinal layers, the findings being considerably different from those related to potent light effect.

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Different degree of sensitivity to acute hypoxia in vivo has been shown in guinea-pig pigmented epithelium, retina and visual cortex Na, K-ATPase. The highest degree of the enzyme activity inhibition has been noted in the pigmented epithelium (more than 3 times), lower inhibition-in visual cortex (26%) and the lowest-in the retina (18%). In contrast to Na, K-ATPase, hypoxia effect on Mg-ATPase resulted in both inhibition and activation of the enzyme in all 3 structures. Reoxygenation following acute hypoxia increases Na, K-ATPase activity inhibition in the retina and visual cortex. But under reoxygenation the enzyme activity is recovered in the pigmented epithelium. Preliminary administrations of vitamin E completely prevented Na, K-ATPase activity inhibition in all studied structures.

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Acute hypoxia was accompanied by intensification of lipid peroxidation in synaptosomal and mitochondrial rat brain fractions as well as by inhibition of Na+, K+- and Mg2+-ATPases. Preadministration of antioxidants vitamin E and ionol into animals prevented distinctly the increase in lipid peroxidation rate, while the ATPases activity was unaltered. Inhibition of the ATPases may be considered as a result of impairing effect of the lipid peroxidation products, which appears to be of importance for structure-functional deteriorations of the nervous system in hypoxia.

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The paper studies intensification of lipid peroxide oxidation in separate brain structures (the medulla oblongata, cerebellum, visual and sensomotor cortex), synaptosomal and mitochondrial fractions under hypoxia. It has been established that acute hypoxia increases accumulation of lipid peroxidation (LPO) products, hydroperoxide and malonyl dialdehyde. Intensification of LPO in synaptosomes and mitochondria is more pronounced as compared to the whole structures. Preliminary treatment with antioxidants (vitamin E and ionol) considerably suppressed LPO intensity under both hypoxia and hypoxia with reoxygenation. Intensification of LPO in synaptosomes and mitochondria is suggested to be the key point in structural-functional disturbances of the nervous system under hypoxia and ischemia.

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The relationship between lipid peroxidation and rat heart mitochondrial monoamine oxidase activity was studied in experimental myocardial necrosis induced by adrenaline injection. It has been established that both the intensity of peroxidation and the activity of monoamine oxidase in mitochondria from adrenaline-injured rat myocardium were essentially increased. The preliminary administration of antioxidants (vitamin E and ionol) was shown to decrease both the intensity of lipid peroxidation and the activity of monoamine oxidase. It is suggested that intensification of lipid peroxidation which is considered to be the main pathogenic factor in ischemic myocardial injury depends on mitochondrial monoamine oxidase activity. Protective effects of antioxidants are realized by the action on two subsequent chains during the formation of active oxygen forms and destruction of lipid peroxidation products.

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Phylo- and ontogenetic aspects of lipid peroxidation and antioxidative enzyme system in the retina of vertebrates were studied. It was established that both the intensity of lipid peroxidation and the activity of glutathione peroxidase in the retina of different vertebrate animals (carp, frog, tortoise, pigeon, rabbit) considerably diminished with evolution. The differences in the intensity of lipid peroxidation and the activity of glutathione peroxidase between dark- and light-adapted retinas also decreased depending on the level of the development. The activity of glutathione peroxidase in the retina of chick embryos was found only at the end of the incubation period.

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Accumulation of lipid peroxidation (LPO) products was investigated in external and internal membranes of mitochondria with anoxia. The increase in LPO intensity in mitochondria membranes during hypoxia was shown to be more expressed in external membranes, with an active involvement of phospholipase A2 in the process revealed. Greater LPO intensity and lability of lysosomal membranes caused by contacts with mitochondria with anoxia have been established.

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The changes in lipid peroxidation of the retina have been investigated during experimental degeneration induced by monoiodoacetic acid and oxygenous intoxication. The results obtained have shown that the development of experimental degeneration of the retina is accompanied by intensification of lipid peroxidation. Injection of vitamin E both before and after monoiodoacetic acid and oxygenous intoxication leads to suppression of lipid peroxidation.

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This work analyses the change of LPO intensity in transplanted skin and in recipient tissue: in blood and skin adjoining the transplants during 27 days after auto- and homotransplantation. A conclusion is made that primary LPO strengthening of autotransplants and skin, adjoining the transplant during 9-14 days after transplantation, growing lesser, reaches the level of intact skin. Under homotransplantation the primary LPO strengthening not only reaches the initial level 9-14 days of the transplantation, but continues to increase. It was shown that the first maximum of LPO strengthening in the transplants (2-5 days after transplantation) were caused by ischemic lesions and the second maximum - by immunologic shifts.

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