Validity and clinical utility of children development assessement using milestones reported by mothers.

INTRODUCTION: The monitoring of infants development during preventive care visits to identify children whose development is concerning for delay is an essential part of pediatric practice. STUDY OBJECTIVE: The aim of the study was to examine the validity and clinical utility of developmental milestones reported by mothers in assessment of children development compared with the outcomes of BSID-II (Bayley Scales of Infant Development--second edition). MATERIAL AND METHODS: The cohort recruited prenatally, included 384 children. The Mental and Motor Scales of BSID-II were administered to each child at the end of the 12th, 24th and 36th month of life. When children were 3 years old, mothers were questioned about their child's age at attainment of 8 significant developmental milestones. RESULTS: Sensitivity for the developmental milestones compared with score on the motor and mental scales of the BSID-II varied from 25.0% to 75.0%, specificity from 54.1% to 80.2%. The all of analysed milestones were characterized by low positive predictive value and rather high the negative one. CONCLUSION: Parent report developmental milestones are a better tool for excluding those children who attain milestones rapidly, as a group with low risk of developmental delays, than in identifying children whose development is suspected of being delayed.

Black-currant protection against oxidative stress formation.

The aim of this study was to investigate the influence of black-currant juice on chronic ethanol-induced oxidative stress and its consequences in liver, brain, and serum of rats. Data demonstrated that administration of black-currant juice to rats improved antioxidant abilities in the examined tissues as evidenced by measurement of activities of Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GSSG-R), as well as levels of glutathione (GSH) and vitamins C, E, and A. Ethanol intoxication produced a decrease in the activities and levels of the antioxidants just listed, and the decrease was accompanied by a reduction in levels of arachidonic acid (AA) and docosahexaenoic acid (DHA). Further results showed enhanced lipid peroxidation as determined by malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), and neuroprostanes and elevated protein levels such as carbonyl groups and dityrosine. Ethanol intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator-activated-receptor (PPARα), AMP-dependent protein kinase (AMPK), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF-α) expression. Administration of black-currant juice to ethanol-intoxicated rats exerted an antioxidant response by restoring to normal quantities the antioxidant levels and enzyme activities and prevented lipid and protein oxidative effects. The activities of alanine transaminase and aspartate transaminase, biomarkers of liver damage, returned to normal after black-currant treatment of ethanol-administered animals. In addition, the expression of PPARα, AMPK, TNF-α, and NFκB confirmed the protective effect of the juice. Data thus indicate the extensive antioxidant metabolic effects of black-currant juice that may be beneficial for humans.

The influence of L-carnitine suplementation on the antioxidative abilities of serum and the central nervous system of ethanol-induced rats.

The brain is exceptionally susceptible to oxidative stress that may be caused by xenobiotics such as ethanol. Alcohol metabolism is accompanied by enhanced free radical formation and a decrease in antioxidant abilities. However, L-carnitine appears to have antioxidant properties and the ability to regulate ethanol metabolism. The present study was designed to estimate the effect of L-carnitine on the antioxidant capacity of the rat brain and blood serum. For 5 weeks during the study, L-carnitine was given to rats in the amount of 1.5 g/1 l of drinking water, and from the second week the rats were intragastrically treated with ethanol. A significant decrease in the activity of antioxidant enzymes (Cu,Zn-SOD, GSH-Px, GSSG-R and CAT) and in the level of non-enzymatic antioxidants (vitamin C, E, A, GSH and GSH-t) as well as a significant increase in the level of GSSG in the brain and blood serum of ethanol intoxicated rats have been demonstrated. It has also been shown that alcohol caused a significant increase in the level of lipid peroxidation products-lipid hydroperoxides, malondialdehyde and 4-hydroxynonenal-and an increase in dityrosine, as well as a decrease in tryptophan-markers of protein oxidative modifications. The administration of L-carnitine to ethanol intoxicated rats partially normalized the activity of the examined enzymes and the level of the above non-enzymatic antioxidants. Moreover, L-carnitine significantly protects lipids and proteins against oxidative modifications. In conclusion, it has been proved that L-carnitine protects rat brain and blood serum against oxidative stress formation and it is possible that this small molecular amine has a similar beneficial effect on the human CNS.

Natural and synthetic antioxidants: an updated overview.

Abstract The current understanding of the complex role of ROS in the organism and pathological sequelae of oxidative stress points to the necessity of comprehensive studies of antioxidant reactivities and interactions with cellular constituents. Studies of antioxidants performed within the COST B-35 action has concerned the search for new natural antioxidants, synthesis of new antioxidant compounds and evaluation and elucidation of mechanisms of action of both natural and synthetic antioxidants. Representative studies presented in the review concern antioxidant properties of various kinds of tea, the search for new antioxidants of herbal origin, modification of tocopherols and their use in combination with selenium and properties of two promising groups of synthetic antioxidants: derivatives of stobadine and derivatives of 1,4-dihydropyridine.

L-Carnitine in the lipid and protein protection against ethanol-induced oxidative stress.

Chronic ethanol intoxication induces oxidative stress participating in the development of many diseases. Nutrition and the interaction of food nutrients with ethanol metabolism may modulate alcohol toxicity. One such compound is l-carnitine (l-3-hydroxy-4-N,N,N-trimethylaminobutyrate), which also reveals antioxidant abilities. The present study has been designed to investigate the effect of l-carnitine as an antioxidant on the serum and liver of rats chronically intoxicated with ethanol. Rats received l-carnitine solution (1.5g/1L) for 5 weeks and/or were treated intragastrically with ethanol for 4 weeks. In the serum and liver, the level of nonenzymatic antioxidants and lipid and protein oxidation markers were determined. It was shown that alcohol caused the increase in the level of lipid peroxidation products-conjugated dienes (by about 70% and 60% in the liver and blood serum, respectively), malondialdehyde (MDA) (by about 60% and 30% in the liver and blood serum, respectively), 4-hydroxynonenal (4-HNE) (by about 35% and 25% in the liver and blood serum, respectively), and changes in the level of protein oxidative markers-increase in dityrosine and decrease in tryptophan (by about 40%) in the serum and liver of rats. Moreover, the decrease in vitamin E level (by about 30%) and the level of glutathione (GSH) (by about 20% in the liver and blood serum) was also observed. Administration of l-carnitine to rats intoxicated with ethanol significantly protects lipids and proteins against oxidative modifications in the serum and liver. The level of conjugated dienes, MDA, and 4-HNE was decreased by about 30%, 30%, and 20% in the liver, respectively, and by about 20%, 10%, and 10% in the blood serum in comparison to the ethanol group. Moreover, the level of tryptophan was increased and dityrosine decreased by about 10% and 20% in the liver, respectively, and by about 30% and 10% in the blood serum in comparison to the ethanol group. l-carnitine partially protects nonenzymatic antioxidants against oxidative stress. The level of vitamin E was increased by about 20% and the level of GSH was increased by about 25% in the liver and blood serum in comparison to the ethanol group. It is possible that beneficial effect of l-carnitine is connected with its abilities to scavenge free radicals and to chelate metal ions.

The Influence of L-Carnitine on Oxidative Modification of LDL In Vitro.

Owing to their structure and function, low-density lipoproteins (LDLs) are particularly susceptible to the oxidative modifications. To prevent against oxidative modification of LDL, L-carnitine, with endogenous small water-soluble quaternary amine possessing antioxidative properties, was used. The aim of this paper was to prove the in vitro influence of L-carnitine on the degree of oxidative modification of the lipid part (estimated by conjugated dienes, lipid hydroperoxides, and malondialdehyde levels) and the protein part (estimated by dityrosine and tryptophan levels) of LDL native and oxidized by cooper ions. The level of lipophylic LDL antioxidant-alpha-tocopherol was also measured.Oxidation of LDL by Cu(2+) enhanced lipid peroxidation. That was manifested by a statistically significant increase in the content of malondialdehyde (threefold), conjugated dienes (up to about 30%), and lipid hydroperoxides (up to about 50%). Cu(2+) ions were also the cause of oxidative modifications of the protein part of LDLs. It was manifested by a significant increase in dityrosine (by about 50%), whereas the level of tryptophan was significantly decreased threefold in relation to native LDL. Incubation of LDL with Cu(2+) ions also caused a significant sixfold decrease of alpha-tocopherol content in oxidized LDL. However, L-carnitine caused a decrease in the level of conjugated dienes, lipid hydroperoxide, malondialdehyde, and dityrosine by about 20% to 30%, and a significant increase (by about 50%) in the content of tryptophan in comparison with oxidative LDL and in a smaller degree significant changes with native LDL. Additionally, L-carnitine caused a significant twofold increase in alpha-tocopherol content in oxidized LDL.The above results indicate that L-carnitine protects the lipid as well as protein part of LDL particles against oxidative modifications, and this natural antioxidant might be used to prevent against diseases of oxidative origin.

[The action of oxidative stress induced by ethanol on the central nervous system (CNS)]. / Wplyw stresu oksydacyjnego indukowanego etanolem na osrodkowy uklad nerwowy (OUN).

The brain is an organ which metabolically consumes about 20% of the total oxygen received by the organism. This causes the generation of free radicals, especially in the presence of some xenobiotics, such as ethanol. In order to prevent free radical-induced cellular damage, the organism developed a defense mechanism, the antioxidative system. The content of both exogenous and endogenous antioxidants in the central nervous system (CNS) is very small in comparison with that of other tissues, which in relation to the high level of polyunsaturated fatty acids (PUFAs) makes the CNS exceptionally susceptible to free-radical damage. The antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GSSG-R) are present in the CNS i.e. in the cortex, cerebellum, hypothalamus, striatum, and spinal cord, where they are responsible for the brain's basic functions, both physical and cognitive. Moreover, the highest activity of these enzymes is observed in neurons and/or glial cells. The activity of antioxidant enzymes is significantly changed in the CNS of animals chronically intoxicated with ethanol. The decrease in these activity may indicate at oxidative modification of the enzymatic proteins caused by free radicals which are generated during ethanol and acetaldehyde metabolism. It may also be caused by the decrease in the synthesis rate of these enzymes. However, the increase in the activity of antioxidant enzymes may often be explained as an adaptive reaction to an excess production of free radicals. The catalase is an exception in this respect because the decrease in its activity is related to the enhancement of protein synthesis. Ethanol intoxication also caused a decrease in GSH concentration, especially in the cerebellum, striatum, and cortex. This may be explained by the increase in the concentration of acetaldehyde, which is removed from cells with the use of this antioxidant. The antioxidative abilities of the CNS also depend on exogenous antioxidants which are provided to the organism during food intake. The most important exogenous antioxidant in the CNS is vitamin E. The content of vitamin E as well as that of vitamin C in the CNS is decreased, whereas the content of vitamin A is increased after ethanol administration. The high vitamin A level may cause damage of the central nervous system, especially in young rats exposed to ethanol in the prenatal period.

Preventive action of green tea from changes in the liver antioxidant abilities of different aged rats intoxicated with ethanol.

OBJECTIVE: The present study investigated the influence of green tea as a source of water-soluble antioxidants on the liver antioxidant potential of different aged rats chronically intoxicated with ethanol. METHODS: Rats (2, 12, and 24 mo old) were fed for 5 wk on a control or an ethanol Lieber-DeCarli diet with and without green tea (7 g/L). The activity and level of enzymatic and non-enzymatic antioxidants and the level of markers of protein and lipid oxidation in the liver of rats were examined. RESULTS: The activities of superoxide dismutase and catalase and levels of vitamins C, E, A, and beta-carotene were significantly decreased, whereas activities of glutathione peroxidase and glutathione reductase and the level of reduced glutathione significantly increased during aging. The ethanol diet caused a significant decrease in activity of antioxidant enzymes and in the level of non-enzymatic antioxidants tested. Administration of green tea to ethanol-treated rats of different ages partly normalized the activity of enzymes and the level of non-enzymatic antioxidants. Changes in antioxidant ability observed during aging were accompanied by increased levels of markers of lipid and protein modifications that also were intensified by ethanol. Green tea caused a decrease in lipid and protein oxidation in aged and ethanol-treated rats. The protective effect of green tea was confirmed by the significantly lower activity of biomarkers of liver damage (alanine and aspartate aminotransferases) in the serum of rats that received green tea with ethanol compared with rats from the control ethanol group. CONCLUSIONS: The use of green tea appears to be beneficial to rat liver by decreasing oxidative stress caused by ethanol and/or aging.

Green tea supplementation in rats of different ages mitigates ethanol-induced changes in brain antioxidant abilities.

Oxidative stress induced by chronic ethanol consumption, particularly in aging subjects, has been implicated in the pathophysiology of many neurodegenerative diseases. Antioxidants with polyphenol structures, such as those contained in green tea, given alone for 5 weeks in liquid Lieber de Carli diet followed by administration with ethanol for 4 weeks with ethanol have been investigated as potential therapeutic antioxidant agents in the brain in rats of three ages (2, 12, and 24 months). Ethanol consumption caused age-dependent decreases in brain superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities. In addition, ethanol consumption caused age-dependent decreases in the levels of GSH, selenium, vitamins, E, A and C, and beta-carotene and increases in the levels of oxidized glutathione (GSSG). Changes in the brain's antioxidative ability were accompanied by enhanced oxidative modification of lipids (increases in lipid hydroperoxides, malondialdehyde, and 4-hydroxynonenal levels) and proteins (increases in carbonyl groups and bistyrosine). Reduced risk of oxidative stress and protection of the central nervous system, particularly in young and adult rats, after green tea supplementation were observed. Green tea partially prevented changes in antioxidant enzymatic as well as nonenzymatic parameters induced by ethanol and enhanced by aging. Administration of green tea significantly protects lipids and proteins against oxidative modifications in the brain tissue of young and adult rats. The beneficial effect of green tea can result from the inhibition of free radical chain reactions generated during ethanol-induced oxidative stress and/or from green tea-induced increases in antioxidative abilities made possible by increases in the activity/concentration of endogenous antioxidants.

[Antioxidative abilities during aging]. / Zdolnosci antyoksydacyjne w starzejacym sie organizmie.

Biological aging is associated with increased cellular levels of reactive oxygen species (ROS) as well as the formation and accumulation of oxidized biomolecules. During evolution, organisms developed a highly-efficient and adaptive antioxidant defense system. Antioxidants can generally be divided into two categories: enzymatic and non-enzymatic. During the aging process the activity of antioxidant enzymes, e.g. SOD, CAT, GSH-Px, and GSSG-R, depends on factors such as race, gender, tissue and subcellular localization of enzymes. The age-dependent decrease in antioxidant enzyme activity may be attributed to oxidative modifications of enzymes. During the aging process, ROS may also lead to the induction of some enzyme activity which is explained as an adaptive phenomenon. The decrease in GSH concentration with age can be explained by decreased GSH synthesis and/or increased GSH consumption in the removal of peroxides and xenobiotics. In plasma albumin, ferritin, transferrin, and caeruloplasmin exert protective action. Plasma proteins can inhibit ROS generation and lipid peroxidation by chelating free transition metals. Plasma protein concentrations changes with age. The major exogenous antioxidants, mostly derived from the diet, are vitamin E, C, A, and beta-carotene. During the aging process the level of vitamins may decrease or increase, depending on such factors as diet, and diseases.