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Biomedical subjects

A M Dupin

Publications and source records attributed to A M Dupin.

At least 19 recordsLinked to original sources
PubMed2001

[Levels and molecular heterogeneity of serotonin transporter protein in platelets of patients with different mental diseases: a comparative analysis with the use of monoclonal and polyclonal antibodies].

Polyclonal (PAb) and monoclonal (MAb) antibodies to CT2-epitope of the C-terminal fragment of serotonin transporter (SERT) protein were used to study the levels and molecular heterogeneity of platelet SERT in healthy donors and patients with affective (AD) and somatoform (SD) disorders, schizoaffective disorder (SAD) and schizophrenia. SERT was found to exist as high molecular wight (HMW) and low molecular weight (LMW) forms separated after electrophoresis. The levels of HMW and LMW forms of SERT were significantly, decreased in mentally ill patients as compared to healthy individuals. Unlike PAb, horse radish peroxidase (HRP)-conjugated MAbs were more sensitive and specific to SERT and could detect the LMW form of SERT as a duplet protein form with MW about 40 and 43 kDa. The MAb to CT2 C-terminal fragment of SERT conjugated with HRP is considered to be a new valuable tool for further investigation of SERT expression, properties, and posttranslation modification in the controls and in patients with different psychopathology.

Adult↗
PubMed2000

[Effect of gangliosides on intensity of the lipid peroxidation process and structural changes in neuronal membranes, caused by toxic doses of glutamate].

We studied effects of gangliosides on the level of lipid peroxides and microviscosity of membrane lipid bilayer in primary dissociated cultures of cerebellar granule cells prepared from 8 day-old rats under conditions of neurotoxic effect of glutamate. It was found that glutamate (100 mkM) treatment of primary cultures activated the processes of lipid peroxidation and decreased microviscosity of neuronal membranes determined as a degree of pyrene excimerization. It was also shown that preincubation of granule cells with gangliosides did not prevent the accumulation of TBA-reactive products induced by glutamate. At the same time gangliosides significantly decreased the membrane-fluidizing effect caused by glutamate.

Animals↗
PubMed1999

[The status of serotonin protein -- a serotonin transporter in thrombocytes in patients with somatoform disorders].

The role of serotonin transporter (SERT) protein in the development of somatoform disorders (SD) was investigated. An association study was performed in terms of the evaluation of the level of SERT immunoreactive (IR-SERT) protein using site-specific antibodies directed at SERT C-terminus fragment, poorly conserved among the other cotransporters. The level of the anxious symptomatology was also estimated in the patients with SD. 22 patients, who met DSM-IV criteria for somatoform disorders, and 32 normals were examined. In platelets from normals, IR-SERT protein migrated as a difuse band between 68 and 105 kDa, and a major sharper band at 43 kDa. Almost complete disappearance of platelet 43 kDa IR-SERT protein band was observed in most of the patients with SD. These findings permitted to suggest a possibility of either biosynthetic or processing abnormality of SERTs in the affected population, that might reflect a dysfunction of serotonin neurotransmission in CNS of the patients with SD.

Adult↗
PubMed1995

Hypoxic and posthypoxic neuronal injury in hippocampal cell culture: attenuation by lipophylic antioxidant U-18 and superoxide dismutase.

The neuroprotective effects of synthesized lipophylic antioxidant from hindered phenol class (U-18) and hydrophylic antioxidative enzyme superoxide dismutase (SOD) were tested on long-term mouse hippocampal cell cultures exposed to hypoxia/reoxygenation. The application of U-18 to the cultures during 6-8 hr hypoxia followed by 16-18 hr reoxygenation in the absence of antioxidant significantly reduced neuronal death. Thus, lipophylic free radical scavenger may exert a delayed neuroprotective effect, probably owing to persistent incorporation into phospholipid membranes and prevention of their lipid peroxidation by means of prolonged intramembranous free radical quenching. On the other hand, the exposure of the cultures to U-18 during 15 hr hypoxia without subsequent reoxygenation also led to significant reduction of neuronal death compared with that observed without antioxidant. These findings suggest that free radical neuronal damage may occur under conditions of prolonged restricted oxygen access to the neurons. The hypoxic/posthypoxic neuronal injury significantly decreased in the cultures exposed to hydrophylic cytoplasmic enzyme SOD (300 U/ml). The neuroprotective effects of both lipophylic U-18 and hydrophylic SOD on the cultures exposed to hypoxia/reoxygenation might reflect the damaging free radical overproduction in different morphofunctional compartments of the nerve cell.

2-Amino-5-phosphonovalerate↗
PubMed1993

The mechanism of interaction of carnosine with superoxide radicals in water solutions.

The antiradical activity and the radiation stability of carnosine in water solutions was studied by the pulse radiolysis technique with spectrophotometric registration of absorbance. The transient spectra were recorded in the range 245-670 nm during 2 x 10(-6)-20 s after the pulse using a flow system for continuous change and saturation of the samples by different gases. Also, the spectra of the stable products of radiolysis were studied. The results obtained give evidence that carnosine in water solutions in the presence of oxygen behaves like a multifunctional antioxidant. Even at low concentrations, dipeptide forms a charge-transfer complex (Car ... O2-., lambda max = 265 nm) with the superoxide radical which changes the reactivity of O2-.. The absorbance band of the complex was shifted towards lower energy as compared to superoxide radical lambda max = 255 nm). The interaction of carnosine with OH-radicals proceeding at very high rate and resulting in the formation of a stable product suggested another type of dipeptide activity. The kinetic mechanism of the interaction of carnosine with products of radiolysis of water in aerobic conditions is discussed.

Carnosine↗
PubMed1993

[A comparison of the antioxidative activity of carnosine by using chemical and biological models].

The difference in the efficiency of carnosine as an antioxidant was found to be explained both by the source of carnosine and the specificity of models used to achieve visualization. Commercial carnosine samples were contaminated with compound (s) absorbing at 255-332 nm. At the same time they possessed better antioxidant activity in the models with Fe2-induced peroxidation process. In the case of chemical models for generation of active forms of oxygen (several modifications of the Fenton reaction) or during burst of superoxide generation by leucocytes, the antioxidant effect of carnosine did not depend of the source of the compound under study.

Animals↗
PubMed1990

[Interactions of carnosine and superoxide radicals in aqueous solutions].

Carnosine was discovered to be able to interact with superoxide-anion and active hydroxyl radicals, using carnosine aqueous solutions. This interaction is specific and can be detected at carnosine concentrations more than 0.02 mM. Interaction of carnosine with O2 results in occurring of charge translocation complex with absorbtion maximum at 265 nm. Stability of this complex is dependent on the medium pH, decreasing with its acidification.

Carnosine↗
PubMed1989

A comparative study of synthetic carnosine analogs as antioxidants.

1. The antioxidative activity of carnosine and 16 related compounds, both synthetic and natural, was determined. 2. The antioxidative effect was estimated by the ability of the dipeptides to prevent MDA accumulation in the course of LPO induced in rabbit sarcoplasmic reticulum membranes by the Fe2+ ascorbate system. 3. It was found that the antioxidative effect comparable to that of carnosine was exerted by water-soluble (cyclo-L-histidyl-L-proline) and alcohol-soluble (cyclo-L-histidyl-L-phenilalanine) dipeptides as well as by the histidine-free cyclodipeptides (cyclo-L-tyrosyl-L-proline). 4. However, in contrast to its synthetic analogs, carnosine not only inhibited the LPO, but also diminished the level of products accumulated during membrane lipid peroxidation.

Animals↗
PubMed1989

[The antioxidant activity of cyclohistidylproline].

A cyclohistidyl-proline, cyclopeptide possessing a hormonal and neurotrophic activity is shown to be an inhibitor of the (Fe + ascorbic acid)-induced peroxidation of membrane lipids, its effect being dependent on its concentration. Inhibition of the malondialdehyde formation by cyclohistidil-proline is accompanied by protection of the membrane bound Ca-pump. In the test of the free radical cumole oxidation antioxidative effect of cyclohistidyl-proline is 4 times higher than that of the hydrophilic antioxidant carnosine. After peritoneal injection of cyclohistidil-proline (15 mg/kg of body weight) to rats the stationary level of thiobarbituric acid reactive products in rat brain or serum is pronouncedly decreased, this effect being in progress up to 6 h after injection. Antioxidative action of cyclohistidyl-proline suggests to be on the basis of a variety of its biological effects.

Animals↗
PubMed1989

[The effect of carnosine on indicators of free radical lipid oxidation during acute stress in rats].

The effect of carnosine intraperitoneal injection in rats (in doses 0.2, 2.0 or 20 mg/kg) on the vegetative parameters (arterial blood pressure, Hildebrandt index), the content of free radical oxidation (FRO) products and superoxide dismutase activity in serum and brain homogenates and brain lipid composition under normal condition and after different stress forms have been investigated. The carnosine injection in dose 20 mg/kg preserves and increase in arterial pressure and Hildebrandt index at all steps of stress development. The phase non-unidirectional changes in studied biochemical parameters have been revealed depending on the level of stress development in animals under control. The unidirectional and dose-dependent changes of phospholipid content and the level of brain lipids, decrease of FRO products in tissue and brain cholesterol, the increase of the superoxide dismutase activity of serum and brain homogenates have been found in intact and stressed animals after carnosine injection. A comparison of carnosine pharmacokinetics with concentration dependences of the antioxidative effect under in vitro and in vivo experiments comes to conclusion concerning the carnosine indirect adaptogenic action.

Acute Disease↗
PubMed1989

[Carnosine prevents the activation of free-radical lipid oxidation during stress].

Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20 mg/kg body weight) induces depletion of lipid peroxidation (LPO) products in brain and blood serum, an increase of superoxide scavenging activity in brain and serum, decrease of cholesterol: phospholipid ratio and increase of easy oxidizable phospholipid portion in brain lipid extracts. After painful stress (footshock during 2 hours) LPO products are accumulated in brain and serum, cholesterol: phospholipid ratio increases and the portion of easy oxidizable phospholipids decreases. Carnosine given before stress prevents LPO activation. Effects of carnosine and stress are not additive: LPO inhibition induced by carnosine is much more in rats subjected to stress.

Animals↗
PubMed1988

Antioxidative properties of histidine-containing dipeptides from skeletal muscles of vertebrates.

1. Ascorbate-dependent peroxidation of lipid components of biological membranes is inhibited by the natural histidine-containing dipeptides, carnosine and anserine, used at physiological concentrations. 2. Carnosine and anserine exhibit an equal antioxidative activity, whereas the preventing effect of homocarnosine is manifested only at low concentrations of oxidized lipid material. 3. The inhibiting effect of the dipeptides is enhanced either by the rise in the dipeptide concentration or by the decrease in the level of membrane components. 4. Addition of the dipeptides results in a marked decrease in the level of primary molecular products of lipid peroxidation. 5. In this case the optical spectrum of primary molecular products of polyunsaturated fatty acids changes significantly.

Animals↗
PubMed1988

The level of natural antioxidant glutathione and histidine-containing dipeptides in skeletal muscles of developing chick embryos.

1. The levels of glutathione and histidine-containing dipeptides in skeletal muscles change in different ways during ontogenesis. 2. The glutathione content in skeletal muscles increases between the 9th and 18th days of embryongenesis--from 0.5 to 2.0 mumol/g of tissue wet wt and then drops to zero in 3-week-old chickens. 3. The level of histidine-containing dipeptides increases throughout the observation period beginning with their appearance on the 14th day in leg muscles and on the 15th day in breast muscles of chicken embryos up to the 21st postnatal day. 4. There is a negative correlation between the antioxidative systems of glutathione and histidine-containing dipeptides in muscle tissue, i.e. dipeptide-rich tissues contain little or no glutathione and vice versa.

Animals↗
PubMed1987

The antioxidative properties of carnosine, a natural histidine containing dipeptide.

The experimental results suggest that the antioxidative function of carnosine is one of the most important manifestations of its biological role. The ability of carnosine to interact directly with lipid peroxidation products was demonstrated. The effects of carnosine on partial restoration of lens transparency in dog eyes with senile cataract which is known to be caused by lipid peroxidation were demonstrated "in vitro" and "in vivo".

Animals↗
PubMed1987

[Muscle dipeptides--natural inhibitors of lipid peroxidation].

The effects of carnosine (beta-alanyl-L-histidine) and anserine (beta-alanyl-1-methyl-L-histidine) on ascorbate-dependent lipid peroxidation in frog skeletal muscle sarcoplasmic reticulum were studied. It was found that the dipeptides (10-50 mM) cause a 25-90% inhibition of ascorbate-dependent lipid peroxidation and decrease the reaction rate and the amount of end products. The nature of lipid peroxidation primary products in the presence of the dipeptides changes which can be evidenced from changes in their spectral properties. Unlike other known natural antioxidants, skeletal muscle dipeptides do not only inhibit lipid peroxidation but also decrease the level of accumulated lipid peroxidation products. Histidine and beta-alanine, similar to imidazole, glycyl-glycine, arginyl-phenyl alanine and alpha-alanyl-D-histidine do not inhibit lipid peroxidation. At the same time, the carnosine stereoisomer D-carnosine which does not exist in nature exhibits a far greater inhibiting effect as compared to its natural counterpart. It is assumed that the skeletal muscle dipeptides carnosine and anserine are highly effective as natural antioxidants.

Animals↗