A. V. Kozlov

Activation of lipid peroxidation in liver mitochondria of hyperthyroid rabbits

If thyroxine is added to medium containing liver mitochondria or homogenates it inhibits lipid peroxidation (LPO) in these systems [2, 5, 6, 9, I0]. Since the doses of the hormone used in these systems were close to physiological (10-6-10 -7 M) and since the antioxidant activity of the hormone was comparable with the ability of ~-tocopherol to slow the rate of LPO processes [2, I0], it was suggested that thyroxine may have a specific function as a natural antioxidant [6]. It is not known, however, whether the fall in the thyroid hormone level leads to activation of LPO reactions or, conversely, to their inhibition at the expense of lipid metabolism. It has been shown that the concentration of a-tocopherol in the serum and liver rises in hyperthyroidism [12]. Meanwhile liver homogenates from hyperthyroid animals in the course of incubation accumulate products reacting with thiobarbituric acid with higher velocities than samples prepared from the liver of normal and hypothyroid animals [13]. Acceleration of LPO reactions in fragments of the sarcop!asmic reticulum in hyperthyroid rabbits also was observed by the present writers previously [3]. Direct addition of thyroxine or other derivatives of the thyroid gland, moreover, is not always accompanied by inhibition of LPO and, on the contrary, it may actually activate LPO, as has been shown in the case of isolated erythrocytes [Ii]. Relations between thyroid hormones and LPO are further complicated by the fact that deiodination of the hormone, considered to be essential for the realization of its biological activity, is increased when the diet is deficient in vitamin E [8], whereas elevation of the bodys thyroid levels leads to an increase in the concentration of this vitamin in the serum and liver.

Regulation of cytochrome c peroxidase activity by nitric oxide and laser irradiation

Apoptosis can be induced by activation of so-called “death receptors” (extrinsic pathway) or multiple apoptotic factors (intrinsic pathway), which leads to release of cytochrome c from mitochondria. This event is considered to be a point of no return in apoptosis. One of the most important events in the development of apoptosis is the enhancement of cytochrome c peroxidase activity upon its interaction with cardiolipin, which modifies the active center of cytochrome c. In the present work, we have investigated the effects of nitric oxide on the cytochrome c peroxidase activity when cytochrome c is bound to cardiolipin or sodium dodecyl sulfate. We have observed that cytochrome c peroxidase activity, distinctly increased due to the presence of anionic lipids, is completely suppressed by nitric oxide. At the same time, nitrosyl complexes of cytochrome c, produced in the interaction with nitric oxide, demonstrated sensitivity to laser irradiation (441 nm) and were photolyzed during irradiation. This decomposition led to partial restoration of cytochrome c peroxidase activity. Finally, we conclude that nitric oxide and laser irradiation may serve as effective instruments for regulating the peroxidase activity of cytochrome c, and, probably, apoptosis.

Ceruloplasmin-transferrin antioxidant system of rats during hyperbaric oxygenation

Hyperbaric oxygenation (HBO) is used in the treatment of several diseases [2, 7]. Meanwhile the use of HBO has some limitations because of the toxic action of oxygen on the patient, which may be due to activation of lipid peroxidation (LPO) in the tissues and, in particular, in the blood serum [2, 6]. For this reason the study of the mechanisms of regulation of LPO processes in the blood serum during HBO is of great interest.

Measurement of the content of Fe(III)-desferal complexes in the perfused rat liver by an EPR method

An important role in the pathogenesis of several diseases is played by disturbances of intracellular iron metabolism [1,2, 5-9]. A number of medicinal preparations are available now which have the ahility to chelate iron ions. The best known of them is desferrioxamine (Desferal) [8, i0, 12]. To estimate the efficacy of binding of intracellular iron by this preparation, a method of determining the quantity of iron chelated within cells must be used.

ROLE OF CERULOPLASMIN, TRANSFERRIN, AND LIPID PEROXIDATION IN BACTERIAL INFECTIONS OF THE CNS

Ceruloplasmin and transferrin blood serum levels were measured during bacterial infection of the CNS. A decrease in ceruloplasmin level and a gradual increase in transferrin level were observed on the 5th day of the disease. The minimum ceruloplasmin level was observed simultaneously with the maximum MDA and GOT levels. There was a close correlation between the time course of ceruloplasmin, transferrin, MDA and GOT changes and the clinical condition of the patient.

Causes of intensification of lipid peroxidation in the blood serum of patients with viral hepatitis B

A central place in the pathogenesis of viral hepatitis B is occupied by the cytolysis syndrome, characterized by increased permeability of hepatocyte cell membranes [9] and an increase in the concentrations of cytoplasmic enzymes and bilirubin in the blood serum [2]. Increased permeability of the cell membranes is associated with intensification of lipid peroxidation (LPO) [4]. Meanwhile, the causes of activation of LPO in hepatitis B are not quite clear. One such cause may be hypoxia [4], whose role in the pathogenesis of hepatitis B is generally familiar [1]. However, the serum LPO level depends on the state of the antioxidative system (AOS) of the blood. The principal components of the AOS of blood serum are cerulo-plasmin (Cp), transferrin (Tf) [11], and a-tocopherol [13]. We studied the causes of accumulation of LPO products in the blood serum of patients with hepatitis B.

Lipid peroxidation and high blood enzyme levels in bacterial diseases of the CNS

: A method for the investigation of cerebral blood flow changes under the influence of vasoactive drugs has been suggested. The method is based on continuous infrared radiation and registration of the reflection from the local brain region through the cerebral cranium. The experiments were conducted on anesthetized cats. The dependence of Pa CO2 on the recorded parameters is shown. The changes in the cerebral blood flow (in conventional units) determined by the alterations of the infrared radiation reflection are shown upon the injection of 1.2 microgram/kg, 2.5 micrograms/kg and 5 micrograms/kg of noradrenaline.

Role of endogenous free iron in activation of lipid peroxidation during ischemia

: Ischemia was simulated in rat liver perfused by physiological solution. The concentration of free iron and lipid peroxidation (LPO) products was measured 1, 2, 3, 4 and 5 hours after ischemia onset. The ESR method was used to measure free iron concentration. The LPO intensity was evaluated by the TBA test and by optical density at 232 nm. The content of free iron in cytoplasm increased in the course of ischemia with an increase in the concentration of LPO products. The content of free iron in the membranes remained unchanged. It is supposed that activation of LPO in ischemia may be caused by the appearance in the cytoplasm of a large amount of free iron. This iron can be liberated from ferritin in conditions of low oxygen concentration.