Biomedical subjects

N Savouré

Publications and source records attributed to N Savouré.

At least 19 recordsLinked to original sources

PubMed1997

Endogenous glutathione as potential protectant against free radicals in the skin of vitamin A deficient mice.

In order to evaluate the relationships between oxidative degradation of lipids and antioxidant defence systems in the skin, weanling female SKH1 hairless mice were randomly divided into two groups. Each group was fed a well-balanced diet, supplemented, in one group with 5 IU vitamin A/g, and vitamin A free in the other, for 20 wk. Liver and plasma vitamin E were increased in mice fed the vitamin A-free diet. Superoxide dismutases, catalase and Se-glutathione peroxidase were determined in dorsal skin homogenates, as well as the concentration of reduced glutathione (GSH) and of thiobarbituric acid-reactive substances (TBARS); the latter is an index of peroxidation of murine skin cell membranes. Vitamin A deficiency did not alter enzyme activities but enhanced the skin reserve of GSH, which appeared to be the reason for a decrease in endogenous lipid peroxidation. Statistical analysis showed a highly significant negative correlation (R2 > 0.6) between the concentrations of TBARS and GSH in these untreated animals. GSH could play a critical role in maintaining a lower background of lipid alteration in the skin of healthy animals and minimizing individual risk.

Animals↗

PubMed1996

Liver transglutaminases and vitamin-A deficiency in hairless mice.

In hairless mice, a moderate vitamin-A deficiency, without any clinical signs or weight changes, reduces the activity of soluble cytoplasmic hepatic transglutaminase without affecting the membrane form of the enzyme. This attack of soluble transglutaminase appears to be a biological marker of early deficiency. The relations between this disturbance and the hepatocyte sensitivity to aggressors at this stage are discussed.

Animals↗

PubMed1996

Modulation of ultraviolet light-induced oxidative stress in mice skin related to dietary vitamin A and selenium intake.

Weanling female SKH1 hairless mice were randomly divided into 4 groups. Each group was fed a particular regimen for 20 weeks: 1) normal basal diet with 5 IU vitamin A/g and 0.45 microgram selenium/g, 2) vitamin A deficient, 3) selenium deficient, and 4) vitamin A plus selenium deficient. Three hours before being sacrificed, half of the animals were subjected to UV A + B irradiation (3 J/cm2). Superoxide dismutases (SOD), catalase, Se glutathione peroxidase activities were determined in dorsal skin homogenates, as well as the concentrations of GSH and of thiobarbituric acid-reactive substances (TBARS), the latter being an index of lipid peroxidation. Ultraviolet light altered the antioxidant defense of mouse skin tissue: GSH level, catalase and Se glutathione peroxidase activities were lowered and SOD was unequally enhanced according to the nutritional status. Vitamin A and Se deficiencies did not perceptibly aggravate the UV-induced oxidative stress, although the former enhanced the decline of catalase expression induced by the irradiation. Probably through an adaptive mechanism, both dietary deficiencies increased the skin reserve of antioxidant GSH and thus appear to modulate the effects caused by reactive oxygen species.

Animals↗

PubMed1995

Vitamin A status and metabolism of cutaneous polyamines in the hairless mouse after UV irradiation: action of beta-carotene and astaxanthin.

Solar radiations (UV A and B) can cause epidermis photoaging and skin cancers. These frequently irreversible effects result from the in situ generation of free radicals. However, it has been noted that nutritional factors can modulate photochemical damage, in particular the common carotenoids present in food, which can be considered as potential prophylactic agents against carcinogenesis. We investigated the effect of UV A and B radiations on the skin of the SKH1 hairless mouse fed a diet either lacking in vitamin A or supplemented with retinol, beta-carotene or astaxanthin. The latter is an oxygenated carotenoid (like canthaxanthin) without provitamin A activity and with strong singlet oxygen quenching ability. After analysing of vitamin status of each group (plasma retinol concentrations and hepatic reserves), we searched for UV-induced modifications of polyamine metabolism by measuring epidermal ornithine decarboxylase (ODC) activity and free polyamines concentration (putrescine, spermidine and spermine). In the basal state without irradiation, differences in ODC activity between groups were nonsignificant; but after UV stimulation, ODC increased markedly in the skin of vitamin A-deficient animals, much more than in other groups. Curiously, the addition of astaxanthin or beta-carotene to the regimen containing retinol reduced the protective effect of retinol alone. Regarding polyamines after irradiation, putrescine was significantly increased in the skin of deficient animals, in parallel with ODC activity. However, astaxanthin had a stronger inhibitory effect on putrescine accumulation than retinol, and decreased spermidine and spermine concentrations: this suggests a specific action on transglutaminases.

Animals↗

PubMed1993

[Vitamins and cancers].

To a great extent carcinogenesis depends on the environment. Some vitamins contribute to the "exogenous" protection against aggressors (i.e., on a molecular scale, active forms of oxygen and free radicals). Epidemiology provides numerous data in favour of this protection, but these date are sometimes ambiguous or contradictory. Current, active experimental studies will probably lead to firm conclusions within the next few years. As regards vitamin A, considerable advances have been made in fundamental research (we now know its molecular mechanism of action, notably on genes) and in applied research (differentiation of leukaemic cells). In various aspects vitamin D resembles vitamin A and also acts on the haematopoietic tissue. Vitamin E is difficult to study, but its protective effect on cell membranes and structures cannot be questioned. Vitamin C emerges from a period of controversy and is increasingly studied at present: it might be a useful adjuvant for the treatment of cancers.

Animals↗

PubMed1993

[Free radicals].

Free radicals are continuously threatening living organs. Firstly generated by endogenic pathway during normal and vital metabolic reactions, they can be also produced by environmental factors: atmospheric pollution, radiations... An energetic source ensures the initiation of free radicals reaction. Its expanding is strengthened by oxygen (bi-radical form) and transition metals (chiefly iron). Eyes are very sensitive organs to the deleterious action from the oxygen active species. Protection systems against free radicals action are necessary in living cells. A part the pathologic or ageing conditions, oxygen toxicity doesn't; in fact, neutralised by protection systems coming from enzymes (endogenic way) and food contribution: vitamins, carotenoids, flavonoids... (exogenic way).

Antioxidants↗

PubMed1993

Hepatic or pulmonary ornithine decarboxylase and vitamin A status in Wistar rat, enzyme kinetics--influence of chloroform.

The ODC activity, initial enzyme in the polyamines synthesis, was studied in the liver and lungs of Wistar rat under avitaminosis A. In the liver: ODC activity is decreased by vitamin A deficiency but partially recovered with retinol repletion during 2 weeks. An intraperitoneal injection of chloroform markedly stimulates the ODC activity, as in the deficient rat as in the normal animal; the response following stimulation is even relatively higher under avitaminosis A. The Km value of ODC increases in the deficiency; intermediate values are obtained in retinol repletion. However the chloroform injection has no effect on the Km values under any of the nutritional state. In the lungs: The baseline ODC activity is slightly decreased in the deficient animals. The chloroform stimulation induced relatively a moderate increase in the normal rat (2 fold over baseline level); it is more intense (4 fold) in deficient animal and the ODC activity is well above those of normally fed control in absolute value. As in the liver, the enzyme Km increases in avitaminosis A and a retinol repletion partially attenuates this influence. Here again, the chloroform stimulation has no effect on the Km values.

Animals↗

PubMed1992

[Toxicity of chloroform and vitamin A status in the rat].

After a chloroform intraperitoneal injection, lactate dehydrogenase, alanine aminotransferase and particularly aspartate aminotransferase serum activities are much more raised in deficient animals. Liver ornithine decarboxylase (ODC) activity normally decreases in rats between the 4th. and the 7th. month after the weaning. In vitamin A deficient animals, basal values of the enzyme activity are lower and the decrease is deeper. But even at month 7, liver sustains a partial capacity of ODC recovery if retinol is fed during 15 days. Chloroform administration strongly enhances liver ODC activity in normal rats. In the deficiency, stimulation is lower in absolute value but relatively higher if referred to basal level. After retinol refeeding, chloroform stimulates enzyme activity to nearly normal values. Vitamin A deficiency impairs obviously liver ODC activity and its response to chloroform stimulation in rats, but the stroke is at least partially reversible in our conditions. Moreover, deficient animals maintain a non negligible capacity of ODC response under chloroform stimulation.

Alanine Transaminase↗

PubMed1987

[Vitamin A status and the carcinogenic action of N-nitrosobenzyl methylamine on the esophagus in the rat].

A state of pure vitamin A deficiency, without any clinical manifestations, rapidly induces a stimulation of ornithine decarboxylase (ODC) activity and some oesophageal mucosal abnormalities (hyperkeratosis, dyskeratosis, cytonuclear abnormalities) in rats treated with N-nitrosobenzylmethylamine (NBMA). Retinol deficient rats fed with retinoïc acid (all-trans) show a mucosal ODC induction, but no morphological lesion. The association of retinoïc acid + retinol, as does retinol alone, prevents simultaneously histological lesions and enzymatic induction. In the liver of vitamin A deficient rats treated with NBMA, a stimulation of the ODC system, without any macroscopical lesions, has been observed.

Animals↗

PubMed1986

[Experimental cancerogenesis. Stimulation of ornithine decarboxylase of the colonic mucosa in vitamin A-deficient rats by sodium desoxycholate].

During a state of pure vitamin A deficiency, without any clinical manifestations, in colonic mucosa: ornithine decarboxylase activity is already stimulated, in deficient animals, by instillation of NaCl 9%. Sodium deoxycholate further enhances and markedly protracts the enzyme activity, as compared to normal rats. These results lead to the conclusion that vitamin A deficiency is a state of special sensibility to the promoter action. Retinol is hence physiologically necessary for natural resistance of intestinal cells against chemically induced tumor promotion.

Animals↗

PubMed1983

[Enzymatic evaluation of blood donors].

Enzymatic, immunologic and hematologic dosages were performed in a group of blood donors. A significant part of this population showed anomalies in the enzymes, either isolated or associated and of variable importance. A systematic serological study of viral hepatitis A (VHA) and viral hepatitis B (VHB) was performed among these donors with biochemical anomalies. A more general biological study (immunology and hematology) completes this work.

Adolescent↗

PubMed1981

Influence of sex hormone binding globulin and serum albumin on the conversion of androstenedione to testosterone by human erythrocytes.

The influence of human serum albumin and sex hormone binding globulin (SHBG) on the enzymic conversion of androstenedione to testosterone in human erythrocytes was investigated in vitro. Total plasma and albumin delayed the conversion rate of androstenedione, while SHBG increased it markedly. The effect of SHBG was largely abolished by heating to 60 degrees C for 1 h and by saturating its binding sites by DHT. The effect of both proteins was found to be related to their concentration. It appears that the binding sites of albumin provide a mechanism for retarding androstenedione uptake by the erythrocytes and that the high binding affinity of SHBG for testosterone facilitates the diffusion of this steroid out of the cell and thus, displaces the chemical equilibrium within the cell.

Androstenedione↗

PubMed1980

[Instability of serum 17 beta-hydroxysteroid dehydrogenases of placental origin].

The stabilization by glycerol of the serum estradiol 17 beta dehydrogenase has been investigated here in terms of time and temperature. The protected enzyme is stable for a month at least at --20 degrees C. Its activity reaches a maximum at 60 degrees C. In another connection, effect of reduced glutathione, of N. acetyl-cysteine and of various mineral ions on the enzymic conversion has been studied.

17-Hydroxysteroid Dehydrogenases↗

PubMed1980

[Comparative activity of erythrocyte 17 beta-hydroxysteroid dehydrogenase in man and the rat: effect of plasma].

Human erythrocytes, which contain an active 17 beta-hydroxysteroid-dehydrogenase, transform dehydroepiandrosterone, delta 4-androstenedione and estrone, more rapidly in buffered medium than when kept into plasma. The rat has a peculiar behaviour: the conversion of substrates is very high above the man's one, whether in buffered medium or in blood: the plasma influence is negligible. Plasma permutation reveals that the rat's one, which does not slow down the erythrocyte activity of the rat, slakens the man's one; the human plasma which slows up the human erythrocyte, has only a light action on the rat's one.

17-Hydroxysteroid Dehydrogenases↗

PubMed1973