Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “alpha-Tocopherol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1979

Contrasts in the actions of protein antibiotics on deoxyribonucleic acid structure and function.

The protein antibiotics neocarzinostain (NCS), macromomycin (MCR), and auromomycin (AUR), which is closely related to MCR, have been compared for their in vitro and in vivo actions on deoxyribonucleic acid (DNA). NCS, markedly stimulated by 2-mercaptoethanol, is much more active in inducing strand scissions in superhelical pMB9 and linear duplex lambda DNA than AUR, which is slightly inhibited by 2-mercaptoethanol. Purified MCR, even at very high levels, does not give any significant amount of cutting with either DNA substrate. 2-Propanol stimulates the activity of NCS but inhibits that of AUR. On the other hand, the antioxidant alpha-tocopherol strongly inhibits DNA breakage by both drugs. The intercalating drugs ethidium bromide, daunorubicin, proflavin, and actinomycin D at low concentrations inhibit DNA scission by AUR. The levels of intercalators required to inhibit NCS activity to comparable levels are about 10 times higher than those for AUR. Although MCR has virtually no in vitro DNA cutting activity, it is, like AUR and NCS, cytotoxic, as measured by the inhibition of DNA synthesis and induction of DNA strand breakage in HeLa cells.

1-Propanol↗
PubMed1978

Activation and inactivation of neocarzinostatin-induced cleavage of DNA.

The possible role of free radicals in the mechanism of neocarzinostatin (NCS) action was studied. While mercaptene markedly stimulate the ability of NCS to degrade DNA, they also rapidly inactivate the antibiotic in a preincubation and at higher concentration inhibit the degradation reaction. The radiation protector S,2-aminoethylisothiuronium bromide-HBr is the most potent compound tested. Scavengers of diffusible OH radicals, O2- or H2O2 do not result in significant inhibition of the oxygen-dependent cleavage of DNA by NCS; in fact, alcohols and other organic solvents stimulate the reaction several-fold. By contrast, the potent peroxyl free radical scavenger, alpha-tocopherol, blocks the reaction 50% at 50 micron.

Alcohols↗
PubMed1975

Inhalation anesthetics and cytochrome P-450-dependent reactions in rat liver microsomes.

The activities of liver microsomal enzymes were studied in preparations from unanesthetized rats and rats anesthetized for one hour with nitrous oxide, diethyl ether, halothane or chloroform. Most of the enzymes studied were cytochrome P-450-dependent oxygenases that hydroxylate endogenous substrates. The other microsomal enzymes, assayed for comparison, included the cytochrome P-450-dependent aminopyrine demethylase, glucose-6-phosphatase, a dehydrogenase, and NADPH-cytochrome P-450 reductase. No anesthetic was associated with a significant change in activity of any enzyme studied. In rats pretreated with phenobarbital no anesthetic except chloroform changed enzymic activity. All hydroxylations were inhibited markedly by chloroform, as were a microsomal dehydrogenation, hydrolysis of glucose-6-phosphate, and NADPH-cytochrome P-450 reductase activity. Administration of alpha-tocopherol did not prevent the inhibition associated with chloroform in phenobarbital-induced animals. It is concluded that cytochrome P-450-dependent hydroxylations involved in metabolic processes normally proceeding in the endoplasmic reticulum of the liver are not permanently affected by the anesthetics used in this study. The inhibitory effect of chloroform after pretreatment with phenobarbital is unspecific and affects a large number of different microsomal enzymes. Evidence that mechanisms other than lipid peroxidation may be responsible for the toxic effects of chloroform in the liver is presented.

Aminopyrine N-Demethylase↗
PubMed2025

CRISPR-Cas9-mediated knockout of OsKCS11 in rice reveals potential crosstalk between very-long-chain fatty acids and cytokinin.

Very-long-chain fatty acids (VLCFAs) play crucial roles in various physiological processes in plants. Through our investigation using a CRISPR-Cas9 knockout mutant library in rice, we identified a semi-dwarf rice mutant named CRISPR-Cas-based dwarf-1 (csd-1). This mutant displayed multiple developmental defects, such as decreased plant height, panicle length, seed size, and seed-setting rate. Whole-genome resequencing analysis revealed that a T-nucleotide insertion in β-ketoacyl-CoA synthase 11 (KCS11), responsible for the initial step in fatty acid elongation, was responsible for the observed defects in csd-1. The identity of csd-1 was confirmed through genetic complementation and CRISPR-Cas9-mediated knockout. Expression analysis indicated that OsKCS11 was present in various tissues, with differential abundance observed through RT-qPCR and promoter GUS staining, and strong localization at the node position by RNA in situ hybridization; furthermore, OsKCS11 protein was confirmed to be in the endoplasmic reticulum. Furthermore, csd-1 exhibited significantly reduced levels of linolenic acid (18:3), C24:0-OH, C28:0-alkanes, C29:0-alkanes, alpha-tocopherol, and C33:0-alkanes, while trans-nonadecenoic acid and behenic acid levels were increased. Cytokinin analysis revealed significant increases in isopentenyladenine (IPA) and cis-zeatin (cZ) levels in csd-1. Molecular investigations indicated upregulation of genes involved in cytokinin biosynthesis or signaling, suggesting a potential link between VLCFAs and cytokinin synthesis through acetyl-CoA. This study not only proposed an alternative gene mapping method based on whole-genome resequencing but also elucidated the mechanism by which VLCFAs influence cytokinin synthesis and signaling.

Oryza↗
PubMed1975

Effect of "drugs for liver disease" on hepatotoxic action of carbon tetrachloride. I. Changes of lysosomal enzyme levels and effect of protoporphyrin on the levels.

In order to clarify the action of drugs for liver disease, the effect of protoporphyrin (PP) on CCl4-induced liver injury was studied. Attention was given to the levels of lysosomal enzymes, some components of the liver, and inhibition of enzymes and lysis of lysosomal membranes by lipid peroxides. Administration of PP to CCl4-poisoned rats was found to prevent the decrease in lysosomal lipolytic enzyme level in the liver, but not in other enzyme levels tested. The inhibition of lipolytic enzyme by CCl4 administered may be partially involved in lipid accumulation in the liver. A dose of PP administered to CCl4-poisoned rats for 8 days depressed the neutral lipid content in the liver nearly to the control value. Methyl linoleate hydroperoxide (hydroperoxide) at a lower concentration of 10(-6)% inhibited the lipolytic enzyme acitivity by 30% and in concentrations ranging from 10(-4) to 10(-3)% inhibited beta-glucuronidase activity. Addition of PP to the medium containing 10(-6) to 10(-5)% hydroperoxide and alpha-tocopherol reduced the enzyme inhibition further than in the absence of PP. The hydroperoxide in concentrations varying from 10(-6) to 10(-3)% caused a partial lysis of liver lysosomal membranes, but addition of PP slightly reduced the damage by the hydroperoxide in concentration lower than 10(-5)%.

Acid Phosphatase↗
PubMed1978

Effects of various compounds on lipid peroxidation mediated by detergent-solubilized rat liver NADPH-cytochrome C reductase.

A reconstituted lipid peroxidation system containing NADPH-cytochrome c reductase isolated from detergent-solubilized rat liver microsomes was used to determine the effects of several compounds, including drugs, on the lipid peroxidation activity. EDTA and ferrous ion were essential requirements for reconstitution of the activity. The addition of 1,10-phenanthroline to the system containing both EDTA and ferrous ion further enhanced the activity. Pyrocatecol, thymol, p-aminophenol, imipramine, p-chloromercuribenzoate (PCMB) and alpha-tocopherol exhibited strong inhibition, aniline, N-monomethylaniline, aminopyrine, benzphetamine, SKF 525-A and NADP exhibited moderate inhibition, and phenol, benzoic acid, acetanilide and nicotinamide exhibited less or no inhibition at the concentrations lower than 1000 micron M. Metal ions such as Hg+, Hg2+, Co2+, Cu2+, Mn2+ and U6+ inhibited lipid peroxidation strongly. In addition, Cd2+, St2+ and Ca2+ exhibited less potent to moderate inhibition, and Ba2+ and Mg2+ were without effects on the activity. Among sulfhydryl compounds tested, dithiothreitol inhibited lipid peroxidation to a greater extent than did the other three compounds, glutathione, cysteine and mercaptoethanol.

Amines↗
PubMed1979

Effect of linoleic acid hydroperoxide on liver microsomal enzymes in vitro.

Rat liver microsomes incubated with linoleic acid hydroperoxide (LAHPO) lost cytochrome P-450 specifically among the enzymes of microsomal electron transport systems. The loss of cytochrome P-450 content and glucose-6-phosphatase activity by LAHPO was accompanied by an increase in malondialdehyde (MDA) production. Turbidity of microsomal suspensions was decreased with increasing MDA production, but not proportionately. Diethyldithiocarbamate (DTC), N,N'-diphenyl-p-phenylenediamine and alpha-tocopherol inhibited almost completely the LAHPO-induced MDA production of microsomes, however no perfect protection against the loss of cytochrome P-450 content and glucose-6-phosphatase activity was observed. The decrease of microsomal turbidity by LAHPO was little affected in the presence of DTC. Purified cytochrome P-450 was destroyed by LAHPO, with minimal protection by the compounds described above. These results suggest the possibility that the loss of microsomal enzyme activities during lipid peroxidation may be attributed largely to a direct attack on enzyme proteins by lipid peroxides rather than indirectly to a structural damage of microsomal membranes resulting from peroxidative breakdown of membrane lipids.

Animals↗
PubMedDate not supplied

[Phytochrome system and synthesis of lipoquinones in the plastids of etiolated hordeum seedlings].

Short pulses of red light induce in etiolated barley seedlings an enhanced synthesis of plastidic benzoquinones and vitamin K1, which can be reverted by subsequent irradiation with short pulses of far-red. As compared to the dark there is more formation of plastoquinone-9 than alpha-tocopherol. The enhanced formation of vitamin K1 is coupled with a concomitant decrease in the level of the second naphthoquinone vitamin "K". The data show that active phytochrome Pfr, also in its ground state, induces the light triggered lipoquinone synthesis which is connected to thylakoid formation. The red light induction of enhanced plastoquinone-9 synthesis cannot be fully reverted by subsequent far-red and seems to be a very fast phytochrome response.

Chlorophyll↗
PubMed1979

[The use of dried grape press cake in pig fattening].

In dried grape press cake the content of crude nutrients and ash, overall sugar, amino acids, alpha-tocopherol and gross energy was determined. In biological experiments with pigs (total of 109 animals) 10% of mixture A1 or SOL was replaced by the same amount of dried crushed grape press cake, without affecting negatively the weight gains and consumption of mixtures per unit of weight gain. Nutritional effects of grape press cake are a subject of discussion and comprise three factors: higher content of enrgy (fat and sugars) in mixtures containing press cake, anti-oxidation effect of press cake and the effect of tocopherols on the metabolism of basic nutrients.

Amino Acids↗
PubMedDate not supplied

[Vitamins K and E and the functional state of connective tissue].

The function of the connective tissue in the skin of albino rats with the vitamin K deficiency was studied. Changes both in the cellular elements and in the fibrous structures (deranged differentiation of cellular elements, changes in the collagenformation, accumulation of acid mucopolysaccarides, etc.) were revealed. All of the mentioned changes are eliminated not only by introduction of vicasol, but also by that of alpha-tocopherol.

Animals↗
PubMed1977

[Damage to the sarcoplasmic reticulum of skeletal muscles in leukemia: role of lipid peroxidation].

Ischemia development was accompanied by inhibition of the enzymatic transport system (ETS) of Ca2+ (reduction of the Ca2+/ATP value and of the Ca2+-dependent ATPase activity), this correlating with the accumulation of primary and secondary molecular products of lipid peroxidation (LPO) in the sarcoplasmic reticulum membranes of the skeletal muscles, in vivo. Administration of antioxidants (2,6-ditretbutyl-4-methylphenol, alpha-tocopherol) prevented the LPO activation in the ischemic muscle and partially protected the ETS of Ca2+ from damage. The blood supply restoration after prolonged ischemia led to further ETS of Ca2+ inhibition against the background of unchanges LPO products level.

Adenosine Triphosphatases↗
PubMed1975

Singlet oxygen production associated with enzyme-catalyzed lipid peroxidation in liver microsomes.

Evidence for the formation of singlet oxygen during the oxidation of NADPH by liver microsomes is presented. The evidence is based primarily on the enzyme-dependent formation of dibenzoylethylene from diphenylfuran, a reaction which is specific for singlet oxygen. The apparent formation of singlet oxygen is coupled to the occurrence of peroxidation of microsomal lipid, a phenomenon known to be associated with NADPH oxidation by the particles. Both the peroxidation of lipid and the apparent formation of singlet oxygen are related to the amount of Fe3+ present in the system and the results are consistent with the possibility that the singlet oxygen formed by this system is derived from the breakdown of lipid peroxides. If 1O2 is formed from breakdown of lipid peroxides, it would be dependent on O-/-2 formation because superoxide anion has been shown to undergo reactions in this system which generate extremely reactive free radicals (probably hydroxyl) that initiate lipid peroxidation. These peroxides are quite unstable and their degradation may be the source of 1O2. We have consistently observed that O-/-2 itself is not a reactive radical with respect to lipids or radical scavengers. Hence, O-/-2 cannot be the radical which initiates lipid peroxidation on which 1O2 generation appears to depend. The results may offer at least part of the explanation for the dietary requirement for alpha-tocopherol which not only scavenges free radicals but quenches singlet oxygen as well. This report also includes description of studies indicating that another enzyme, xanthine oxidase, which forms superoxide anion during its activity under aerobic conditions, does not form singlet oxygen during its function. This finding is in contrast to reports of others which indicate that xanthine oxidase activity does produce 1O2.

Aniline Compounds↗
PubMed1978

[Mechanism of brain Na,K-ATPase activation by adrenaline].

Norepinephrine stimulates Na, K-ATPase from rat brain homogenates at concentrations of 10(-4)--10(-5) and 10(-7)--10(-8) M. A low concentration maximum is observed after 48 hrs of incubation at -20 degrees C and is not changed by the addition of alpha-tocopherol, glycerol and MAO inhibitor ipraside. The maximum observed at the mediator concentration equal to 10(-4)--10(-5) M is eliminated after treatment with EGTA. At all concentrations of norepinephrine the enzyme stimulation is removed by the alpha-adrenoblocker phentolamine. The activated enzyme reveals lower sensitivity to Ca2+ induced inhibition. The role of Ca2+ and conformational state of the membranes in the realization of the remote effect on the adrenoreceptor-Na, K-ATPase system is discussed.

Animals↗
PubMed1977

Antioxidant function of vitamin A.

Feeding of 100 000 I.U. of Vitamin A on alternate days, five times to rats, resulted in a marked lowering in in vitro lipid peroxidation of the tissue hemogenates. alpha-Tocopherol or DPPD supplementation along with A still further reduced the in vitro lipid peroxidation of the tissues. Vitamin A in large doses increased the antioxygenic potential of the tissues, and it is suggested that retinol also might be considered as a potential antioxidant similar to tocopherol in animal nutrition.

Alopecia↗
PubMed1978

[Action of vitamin D and E on the erythrocyte membrane. II. Morphological changes in the erythrocytes studied by transmission electron microscopy].

Man, rabbit, guinea-pig erythrocytes treated "in vitro" with high doses of cholecalcipherol or alpha-tocopherol release K+ and haemoglobin and show ultrastructural damages. These damages consist in a change of the red cells profile as well as in the desappearance of the glycocalix, in alterations of the membrane and of the cortical cytoplasm structure. These ultrastructural alterations are of a different degree, depending on the animal species; they partly resemble the erythrocyte changes induced by retinol. Our results are in partial agreement with the Dingle and Lucy's hypothesis on the common action of liposoluble vitamines on the erythrocyte membrane.

Animals↗
PubMed1978

[Effect of vitamin D and vitamin E on the erythrocyte membrane. I. Effect on in vitro osmolar resistance and lysis].

As in the case of retinol, low doses of cholecalcipherol and alpha-tocopherol "in vitro" increase the osmotic resistance of red blood cells, while high doses have a lytic effect on the erythrocytes of various animal species (e.g.: man, sheep, rabbit, guinea-pig, mouse, rat) with the exception of the chicken. The haemolytic effect of cholecalcipherol is less intense than that of retinol; alpha-tochopherol, while causing even less haemolysis than cholecalcipherol, involves a remarkable loss of K+ from the red cells. Besides these quantitative differences, the mechanism of action of the three vitamins seems somewhat different, as shown by modifications of the suspension medium (e.g.: pH, temperature, presence of proteins and reducing substances) or by treatment of the red cells with trypsin. Our results therefore essentially confirm the hypothesis of Dingle and Lucy of common mechanism of action of liposoluble vitamins on biological membranes.

Cholecalciferol↗
PubMedDate not supplied

Comparison of hepatic microsomal drug-metabolizing systems from rats fed crude and purified diets.

Hepatic microsomes from rats fed a crude or a purified diet were compared by measureing their contents of protein, cytochrome P-450, and cytochrome b5, their rates of activity of NADPH- and NADH-cytochrome c reductases, NADPH-cytochrome P-450 reductase, NADPH oxidase, lipid peroxidase, ethylmorphine N-demethylase, aniline hydroxylase, benzpyrene hydroxylase, and their substrate-binding spectra (ethylmorphine, hexobarbital, aniline, and ethyl isoyanide). With the exception of lipid peroxidase activity, which was much higher in microsomes from animals fed the crude diet, little or no consistent diet-related differences in these measurements were observed over a 4-week experimental period, nor were results significantly less variable with one or the other diet. No consistent significant differences were observed with two strains of rats. The lower lipid peroxidase activity seen with the purified diet appeared to be due to the high vitamin E intake when that diet was employed; rats fed the crude diet and an oral supplement of alpha-tocopherol yielded microsomes with low lipid peroxidase activities similar to those seen in microsomes from rats fed the purified diet. A gradual temporal increase in benzpyrene hydroxylase activity was observed with both diets. This was interpreted to be due to environment inducing agents other than those present in the diet.

Analysis of Variance↗
PubMed1978

Inhibition of ultraviolet and phototoxic dermatitis in the mouse.

The effect of inhibitors on the inflammatory oedema elicited by medium-wave ultraviolet radiation (UVB) and long-wave ultraviolet radiation (UVA) in combination with chlorpromazine has been studied in the mouse, by means of a quantitative technique. Inhibition of the UVB reaction was observed with indomethacin, acetylsalicylic acid and betamethasone valerate, whereas the latter compound only was effective in the phototoxic state. No inhibition was obtained with hydrocortisone, phenylbutazone, epsilon-aminocaproic acid, polyphloretin phosphate, clemastin, alpha-tocopherol or ascorbic acid. With indomethacin and betamethasone valerate there was no inhibition at high doses when the compound was administered before UVB irradiation. These results are in accordance with a proposed central role for the prostaglandins in UVB inflammation. It is suggested that the phototoxic reaction to chlorpromazine may not be due to mediator action but rather to the effect of toxic photoproducts.

Animals↗