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M Clément

Publications and source records attributed to M Clément.

At least 37 records · Page 2Linked to original sources
PubMed1996

Influence of a dietary alpha-linolenic acid deficiency on learning in the Morris water maze and on the effects of morphine.

Female OF1 mice were fed on a diet deficient in alpha-linolenic acid or on a control diet 3 weeks before mating and throughout pregnancy and lactation. Pups fed on the same diet as their mothers were used for experiments. The effects of dietary alpha-linolenic acid deficiency were studied in a model of learning, the Morris water maze, and on the following effects of morphine: increase in locomotor activity, modifications of rectal temperature and analgesia. In the place and in the cue versions of the Morris water maze, learning occurred at the same speed in the two diet groups; however, in the place version of the test, the level of the performance was significantly lower in the deficient mice. The probe trial and the extinction procedure did not show any difference between the two diet groups. The morphine-induced increase in locomotor activity occurred significantly earlier and was greater in the deficient diet group. Morphine induced an early hypothermia followed by a late hyperthermia; the hypothermia was significantly greater and the hyperthermia significantly smaller in the deficient mice. The pain thresholds and the morphine-induced analgesia were unmodified by the dietary deficiency. The plasma levels of morphine were similar in the two diet groups.

Analgesics, Opioid↗
PubMed1996

[Vitamin E: comparison of efficiency of incorporation of alpha-tocopherol in the organs in comparison to gamma-tocopherol].

Refeeding rats deficient in vitamin E with alpha-tocopherol induces increased amount of this compound in brain, cerebellum, sciatic nerve and muscle. This increase is regular with time. The optimum level (corresponding to non-deficient animals) is not reached within 8 weeks after refeeding. Thus recovery is very slow for the nervous tissue (as it has been demonstrated for polyunsaturated fatty acids). In contrast, the optimum level is reached within 2 weeks for liver and serum. Refeeding rat deficient in vitamin E with gamma-tocopherol induces an increase of this compound in the liver, the plateau is reached within 2 weeks, but is clearly lower than the one obtained with alpha-tocopherol : approximately 4 times lower. In the muscle, the uptake is linear with time, the plateau is not reached within 8 weeks, its level is 4 times lower than with alpha-tocopherol. Important point : feeding animals deficient in vitamin E with gamma-tocopherol induces in the nervous system a level of gamma-tocopherol which is not the one of the residual alpha-tocopherol; the plateau is not reached within 8 weeks. In sciatic nerve and cerebellum (but not in the brain) increased amount of gamma-tocopherol as a function of time is parallel with a slight but significant reduction of the residual alpha-tocopherol. In another experiment, rats were fed a diet deficient with vitamin E until 60 days of age. From this age, they received a non deficient diet until 120 days. In all organs, increasing the ratio gamma/alpha tocopherol (with a constant amount of alpha-tocopherol) induces an increase of alpha-tocopherol. This result is unexpected, as it was possible to propose that gamma-tocopherol could reduce alpha-tocopherol utilisation by competition. Conversely, the presence of alpha-tocopherol seems to increase incorporation of gamma-tocopherol, except in brain and sciatic nerve. The presence of gamma-tocopherol seems to induce increased need of alpha-tocopherol. This specificity for alpha-tocopherol is very important in terms of nutrition and pharmacology. In fact, at least to preserve biological membranes, it is important to provide only alpha-tocopherol, and not other molecules.

Animals↗
PubMed1995

Uptake of dietary RRR-alpha- and RRR-gamma-tocopherol by nervous tissues, liver and muscle in vitamin-E-deficient rats.

The time course of RRR-alpha-tocopherol and RRR-gamma-tocopherol uptake by liver, muscle and selected nervous tissues was studied in vitamin-E-deficient rats fed diets containing either RRR-alpha-tocopherol or RRR-gamma-tocopherol over a 60 day period. Feeding rats with a RRR-alpha-tocopherol-supplemented diet induced in brain, cerebellum, sciatic endoneurium and muscle a marked and regular increase in alpha-tocopherol concentration. In addition, the tocopherol concentration in liver reached a plateau very rapidly. In contrast, feeding rats with a diet containing the same level of RRR-gamma-tocopherol induced a very small increase in gamma-tocopherol concentration in brain, cerebellum, sciatic endoneurium and muscle, no change in alpha-tocopherol concentration of brain and muscle and a slight but significant decrease in alpha-tocopherol concentration in sciatic endoneurium and cerebellum. These results indicate that when gamma-tocopherol was supplied continuously in the diet gamma-tocopherol accumulated significantly in the tissues but to a much lesser extent than when rats were fed with RRR-alpha-tocopherol. These results also show that in the tocopherol-deficient rat, gamma-tocopherol does not significantly affect the residual alpha-tocopherol concentrations in brain or cerebellum, except poorly in sciatic endoneurium.

Animals↗
PubMed1995

[Adoption of health promotion behaviors in first-year baccalaureate nursing students: pilot study].

The goal of this pilot study was to test the usefulness of Pender's (1987) theoretical model in predicting the adoption of health-promotion behaviours in 176 first-year undergraduate nursing students. Hierarchical regression analysis indicated that the perception of self-efficacy, perception of one's state of health, the influence of professors, and place of birth are predictive variables of health-promoting behaviours in this group. The results of this study suggest, among other things, that it is important for professors to use strategies that foster and support students' confidence in their ability to commit to health-promoting behaviours. A longitudinal study currently in progress will examine whether a health-oriented program significantly influences the adoption of health-promotion behaviours in nursing students during their university education.

Adolescent↗
PubMed1993

Function of dietary polyunsaturated fatty acids in the nervous system.

The brain is the organ with the second greatest concentration of lipids; they are directly involved in the functioning of membranes. Brain development is genetically programmed; it is therefore necessary to ensure that nerve cells receive an adequate supply of lipids during their differentiation and multiplication. Indeed the effects of polyunsaturated fatty acid (PUFA) deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid (LA) is now universally recognized to be an essential nutrient. On the other hand, alpha-linolenic acid (ALNA) was considered non-essential until recently, and its role needs further studies. In our experiments, feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs in reduced amounts of 22:6(n-3), compensated by an increase in 22:5(n-6). The speed of recuperation from these anomalies is extremely slow for brain cells, organelles and microvessels, in contrast with other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na-K-ATPase of nerve terminals and a 20% reduction in 5'-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in ALNA induces alterations in the electroretinogram which disappear with age: motor function and activity are little affected but learning behaviour is markedly altered. The presence of ALNA in the diet confers a greater resistance to certain neurotoxic agents, i.e. triethyl-lead. We have shown that during the period of cerebral development, there is a linear relationship between brain content of (n-3) acids and the (n-3) content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g food intake. Beyond that level there is a plateau. For the other organs, such as the liver, the relationship is also linear up to 200 mg/100 g, but then there is merely an abrupt change in slope and not a plateau. By varying the dietary 18:2(n-6) content, it was noted that 20:4(n-6) optimum values were obtained at 150 mg/100 g for all nerve structures, at 300 mg for testicle and muscle, 800 mg for the kidney, and 1200 mg for the liver, lung and heart. A deficiency in ALNA or an excess of LA has the same main effect: an increase in 22:5(n-6) levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Alteration in 5'-nucleotidase activities and composition of liver and brain microsomes of developing rats fed different dietary fats.

Four groups of male weanling rats were fed during three months, diets different in the nature of fats and the activity of 5' nucleotidase and fatty acid composition of brain and liver microsomes were studied. Group A were fed a standard commercial diet, group B a fat free-diet and group C and D a fat free-diet, containing respectively 10% of peanut-rapeseed oil and 10% of salmon oil. In brain and liver microsomes, 5'-nucleotidase activity increased throughout the development for all diets (except for the fat-free diet). Slight differences were found in rats fed the peanut-rapeseed oil diet compared to controls estimated at the same time. However, in animals fed the fish-oil diet, 5' nucleotidase had the highest activity in both brain and liver microsomes. Marked changes occurred in the fatty acid patterns of brain and liver microsomes among the various groups. The greatest alterations were found in the liver microsomes. In brain and liver microsomal membranes the fat-free diet induced an increase in monounsaturated fatty acids, an synthesis of eicosatrienoic acid, and a decrease in (n-6) and (n-3) polyunsaturated fatty acids. Animals fed a peanut-rapeseed oil and control diet showed similar fatty acid patterns in liver and brain microsomes. However, when rats were fed a fish-oil diet, the liver microsomal membranes were highly enriched in eicosapentaenoic and docosahexaenoic acids, and simultaneously there was a decrease in arachidonic acid. These results suggest that manipulation of the lipid environment influences 5'-nucleotidase activity by the interaction of the enzyme with specific membrane lipids.

5'-Nucleotidase↗
PubMed1992

Alteration of delta-6 desaturase by vitamin E in rat brain and liver.

delta-6 Desaturase, measured at substrate saturation using linoleic acid, was found to be increased by more than two-fold when the content of vitamin E in brain microsomal membrane suspension was increased (up to 7.5 micrograms/mg membrane protein, i.e. 100 micrograms/g tissue from which microsomes were prepared). In contrast, this activity was reduced by 25% in the liver. This raises the question of the multiple role of vitamin E in membranes, the control of membrane polyunsaturated fatty acids through synthesis, and their protection against peroxidation.

Animals↗
PubMed1992

Structural and functional importance of dietary polyunsaturated fatty acids in the nervous system.

The nervous system is the organ with the second greatest concentration of lipids. These lipids participate directly in membrane functioning. Brain development is genetically programmed. It is therefore necessary to ensure that nerve cells receive an adequate supply of nutrients, especially of lipids, during their differentiation and multiplication, and throughout their lives. The effects of polyunsaturated fatty acid deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid is now universally recognized to be an essential nutrient. Until recently, however, alpha-linolenic acid was considered non-essential. Feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs having reduced amounts of 22:6n-3, which is compensated for by an increase in 22:5n-6. The speed of recuperation from these anomalies is extremely slow for brain cells, organelles, and microvessels, in contrast to other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na(+)-K(+)-ATPase of nerve terminals and a 20% reduction in 5'-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in alpha-linolenic acid induces alterations in the electroretinogram which disappear with age; motor function and activity are little affected, but learning behavior is markedly altered. The presence of alpha-linolenic acid in the diet confers a greater resistance to certain neurotoxic agents (triethyl-lead). During the period of cerebral development, there is a linear relationship between brain content of n-3 acids and the n-3 content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g of food intake. Beyond that level there is a plateau. For other organs, such as the liver, the relationship is also linear up to 200 mg/100 g, but then there is merely an abrupt change in slope and not a plateau. When dietary 18:2n-6 content was varied, it was noted that 20:4n-6 optimum values were obtained at 150 mg/100 g for all nerve structures, 300 mg for testicle and muscle, 800 mg for kidney, and 1200 mg for liver, lung and heart. A deficiency in alpha-linolenic acid and an excess of linoleic acid have the same main effect: an increase in 22:5n-6 levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Age-related changes in antioxidant enzymes and lipid peroxidation in brains of control and transgenic mice overexpressing copper-zinc superoxide dismutase.

The aim of our study was first to obtain a comprehensive profile of the brain antioxidant defense potential and peroxidative damage during aging. We investigated copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), seleno-dependent glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R) activities, endogenous and in vitro stimulated lipid peroxidation in 40 brains of control mice divided into 3 age groups: 2 months (young), 12 months (middle-aged) and 28 months (old). We found a positive correlation between age and activities of CuZnSOD (r = 0.47; P < 0.01) and GSH-PX (r = 0.72; P < 0.0001). CuZnSOD and GSH-PX activities are independently regulated during brain aging since temporal changes of these two enzymes do not correlate. No modification in MnSOD activity and basal lipid peroxidation was observed as a function of age. Nevertheless, stimulated lipid peroxidation was significantly higher at 12 months (6.53 +/- 0.71 mumole MDA/g tissue) than at 2 months (5.69 +/- 0.90) and significantly lower at 28 months (5.13 +/- 0.33) than at 12 months. Second, we used genetic manipulations to construct transgenic mice that specifically overexpress CuZnSOD to understand the role of CuZnSOD in neuronal aging. The human CuZnSOD transgene expression was stable during aging. The increased CuZnSOD activity in the brain (1.9-fold) of transgenic mice resulted in an enhanced rate of basal lipid peroxidation and in increased MnSOD activity in the 3 age groups. Other antioxidant enzymes did not exhibit modifications indicating the independence of the regulation between CuZnSOD and glutathione-related enzymes probably due to their different cellular localization in the brain.

Aging↗
PubMed1990

Precursors for cholesterol synthesis (7-dehydrocholesterol, 7-dehydrodesmosterol, and desmosterol): cholesterol/7-dehydrocholesterol ratio as an index of development and aging in PNS but not in CNS.

In rat sciatic nerve, the 7-dehydrocholesterol content decreased dramatically during the postnatal period and slowly during adulthood and aging. In contrast, the 7-dehydrodesmosterol content peaked at 14 days and was nearly undetectable after 60 days. The desmosterol content peaked at 21 days and was nearly undetectable after 1 year. The cholesterol content increased up to 21 days and remained nearly constant thereafter. In brain (in contrast to sciatic nerve), 7-dehydrodesmosterol and desmosterol contents decreased dramatically during development and slightly during adulthood and aging; the 7-dehydrocholesterol content peaked at 21 days and remained constant during aging. Only 7-dehydrocholesterol was dramatically more concentrated in PNS than in CNS. In brain, the cholesterol/7-dehydrocholesterol ratio increased during development and remained stable after 6 months. In contrast, in sciatic nerve, this ratio continuously increased during development and aging (950-fold between 5 days and 18 months). Thus, the cholesterol/7-dehydrocholesterol ratio is a useful biochemical index of development and aging in the PNS.

Aging↗
PubMed1990

Alteration of alpha-tocopherol content in the developing and aging peripheral nervous system: persistence of high correlations with total and specific (n-6) polyunsaturated fatty acids.

In contrast to brain, the sciatic nerve concentration of vitamin E in rats increased rapidly during the postnatal period (approximately fivefold between days 1 and 8), then decreased dramatically (about twofold between days 8 and 30), and further decreased slowly between days 30 and 60 and remained constant up to 2 years. Although the sciatic nerve concentration of vitamin E decreased by 58% between days 8 and 30, the concentration of vitamin E in serum presented a marked decrease (approximately 75%). The vitamin E concentrations varied in a similar pattern in whole sciatic nerve and in endoneurium and showed a very close correlation (r = 0.94). The age-related changes in fatty acid concentration of the endoneurial fraction of the sciatic nerve were characterized by a large increase in content of saturated and monounsaturated fatty acids up to 6 months (twofold for saturated and fourfold for monounsaturated fatty acids). Then, up to 24 months, the amount of these fatty acids decreased very slowly. The content of (n-6) polyunsaturated fatty acids (PUFAs) decreased rapidly up to 1 year and slowly afterward. In contrast, during development the amount of (n-3) PUFA was relatively stable and decreased during aging. A highly significant correlation between vitamin E and (n-6) PUFA [18:2(n-6), 20:4(n-6), and total (n-6)] was observed but not between (n-3) PUFA and vitamin E. It is suggested that there may be a relationship between vitamin E and (n-6) PUFA in the PNS membranes during development and aging.

Aging↗
PubMed1990

T3 plus high doses of beta-blockers: effects on energy intake, body composition, bat and heart in rats.

The effects of a combined treatment with supraphysiological doses of the thyroid hormone T3 (15 micrograms/kg BW/day, s.c.) and high doses of a predominant beta 1-blocker (atenolol, 12.5 and 25 mg/kg BW, 3X/day, s.c.) or a non-specific beta-blocker (propranolol, 5 mg/kg BW s.c. and 33 mg/kg BW p.o., each 3X/day) on energy intake, body composition and the heart were studied in overfed rats with an increased body fat content. The goal of the study was to investigate whether the above treatment constitutes a therapy for obesity in that T3 causes weight and fat loss and the beta-blockers prevent the unwanted T3-effects on the heart (tachycardia and increased heart weight). T3 did not increase energy intake above the level seen in overfed animals. It caused loss of body weight due to loss of fat but not protein, an increase in interscapular brown adipose tissue (IBAT) weight and fat, tachycardia and an increase in heart weight. Atenolol and propranolol blocked T3-induced tachycardia. With the exception of the highest propranolol dose which abolished the T3-induced increase in IBAT fat content, the beta-blockers did not modify the other T3 effects. Thus, in spite of the weight and fat loss and the lack of significant protein loss and tachycardia observed under T3/high dose beta-blockers treatment, the T3-induced increase in heart weight makes this treatment unsuitable as a therapy for obesity.

Adipose Tissue↗
PubMed1989

Alterations of cholesterol synthesis precursors (7-dehydrocholesterol, 7-dehydrodesmosterol, desmosterol) in dysmyelinating neurological mutant mouse (quaking, shiverer and trembler) in the PNS and the CNS.

In brain, levels of cholesterol, desmosterol and 7-dehydrodesmosterol are reduced in shiverer and quaking, but not in trembler 60-day-old dysmyelinating mutant mice. Very interestingly, 7-dehydrocholesterol is not altered in any mutant. The amount of cholesterol is similar in the different normal control mouse strains and in rat. In contrast, levels of precursors are not the same. In sciatic nerve, cholesterol is slightly reduced in shiverer, reduced 2-fold in quaking, and dramatically reduced in trembler (10-fold). 7-Dehydrocholesterol is affected in all mutants.

Animals↗
PubMed1989

Antioxidant enzymes and related trace elements in aging brain capillaries and choroid plexus.

The activities of superoxide dismutase (SOD), glutathione peroxidase, glutathione reductase, and catalase were measured in isolated brain capillaries, choroid plexus, cerebrum, and cerebellum from rats of 2, 6, 12, and 24 months. The contents of copper, zinc, and manganese were determined in capillaries, cerebrum, and cerebellum, and the profile of fatty acids was studied in brain capillaries. In brain capillaries, the activities of glutathione peroxidase and glutathione reductase did not change with age. The activities of the two enzymes increased in cerebrum and cerebellum. In choroid plexus, glutathione peroxidase activity increased, but glutathione reductase activity remained unchanged. Catalase activity in brain capillaries declined, whereas in choroid plexus, cerebrum, and cerebellum, it did not change. The activities of the three enzymes were significantly higher in brain capillaries and choroid plexus than in cerebrum and cerebellum. SOD activity increased in the four tissues. Copper content in the capillaries increased initially and then levelled off, whereas it continued to increase in cerebrum and cerebellum. Zinc increased in brain capillaries, but did not vary in cerebrum and cerebellum. Manganese content remained constant in all tissues studied. The percent of saturated fatty acids in brain capillaries did not change with age, whereas those of mono- and polyunsaturated fatty acids increased and decreased, respectively. The possibility that a deficiency of enzymes protective against free radicals causes blood-brain barrier and blood-cerebrospinal fluid barrier degeneration is ruled out.

Aging↗
PubMed1987

Unaltered brain membranes after prolonged intake of highly oxidizable long-chain fatty acids of the (n-3) series.

Feeding rats a diet enriched in n-3 polyunsaturated fatty acids (Menhaden oil) increased the content in eicosapentaenoic acid 20:5 n-3 of brain phospholipids. Conversely 22:4 n-6 was reduced. These changes were not associated with alterations in either vitamin E concentration or glutathione peroxidase and catalase activities in cerebrum and cerebellum. No increase in peroxidative damage was found. Interestingly the major very-long-chain fatty acids (22:6 n-3 and 22:5 n-3) were not affected.

Animals↗
PubMed1983

Hepatic lipid peroxidation and mitochondrial susceptibility to peroxidative attacks during ethanol inhalation and withdrawal.

Male Sprague-Dawley rats were exposed to increasing concentrations (15-22 mg/l) of ethanol vapor over a 4-day period. The hepatic lipid peroxide level as well as the sensitivity of mitochondria and microsomes to peroxidative attacks were studied during the early stage of alcohol intoxication, at the end of the inhalation period and, finally, during withdrawal. The level of hepatic lipid peroxide started to increase significantly after the first day of ethanol inhalation, whereas the in vitro mitochondrial sensitivity to peroxidation induced by ADP X Fe3+ in the presence of an O(2)-generating system was still unaltered after a 2-day inhalation period. Both the hepatic peroxide level and the mitochondrial sensitivity to peroxidation were significantly enhanced at the end of the 4-day inhalation period. Such an enhancement was still apparent 24 h after withdrawal, a time at which no more ethanol was present in the blood. Lipid peroxidation returned to normal values only 48 h after withdrawal. Microsomes were less affected than mitochondria by the ethanol treatment. It is suggested that the alterations of lipid peroxidation are related to the presence and/or the metabolism of ethanol at an early stage of inhalation, whereas changes in the membrane structure would be responsible for the maintenance of enhanced lipid peroxidation 24 h after ethanol withdrawal.

Animals↗