PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Malondialdehyde”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1979

Dissociation between prostaglandin and malondialdehyde formation in exudate and increased levels of malondialdehyde in plasma and liver during granulomatous inflammation in the rat.

During kaolin-induced granuloma pouch inflammation in the rat the concentration of malondialdehyde (MDA) in the exudate, measured by the 2-thiobarbiturate method, steadily increased and this increase was correlated with the increase in granuloma weight. There was a complete lack of correlation between the concentrations of MDA and prostaglandin (PG)-like material in the inflammatory exudate. Whereas the concentration of PGs reached a maximum 1 day after the induction of inflammation and returned to control levels on day 4, the MDA concentration continuously increased from the initiation of inflammation up to day 16. During granuloma development the concentration of MDA in the plasma reached a maximum on day 2 in parallel with the concentration in the liver, then both plasma and liver MDA decreased to levels observed in control rats. Between day 2 and 8 of the inflammatory process homogenates of livers from inflamed rats showed an increased formation of MDA on incubation, the amount formed being maximal on day 4. The results of the present study are discussed in view of a possible involvement of lipid peroxidation in inflammation.

Animals↗
PubMed1992

[Ischemia and reperfusion: the production and release of malondialdehyde, oxypurines and nucleosides in the isolated rat heart].

Ischemia and reperfusion damage has been evaluated by determining the sum of adenine nucleotides, nucleosides, oxypurines and the concentration of malondialdehyde, ascorbic acid, lactate and pyruvate in the isolated rat heart subjected to global normothermic ischemia and subsequent reperfusion. In addition, the sum of oxypurines and nucleosides, and the concentration of malondialdehyde has been determined in the perfusate collected during the reperfusion. Data indicate that ischemia and reperfusion induce an oxidative stress to myocardial tissue (increase of tissue malondialdehyde and decrease of ascorbic acid, and release of malondialdehyde during reperfusion) that, due to the output of relevant amount of oxypurines (congruent to 6.7 mumol/g dry weight) and of nucleosides (congruent to 7.0 mumol/30/min/g dry weight), it is not even able to restore its energy metabolism after reperfusion.

Animals↗
PubMed1976

Malondialdehyde formation as an indicator of prostaglandin production by human platelets.

The formation of malondialdehyde, a metabolite of prostaglandin endoperoxides, has been studied in platelet-rich plasma. Small amounts were produced in response to ADP, epinephrine, or collagen and larger amounts in response to thrombin. Arachidonic acid induced platelets to produce large amounts of malondialdehyde. Malondialdehyde formation by platelets was prevented by aspirin or indomethacin. The measurement of malondialdehyde in platelet-rich plasma may be used as an indicator of platelet prostaglandin synthesis, and is simpler than the measurement of prostaglandins.

Adenosine Diphosphate↗
PubMed1977

Malondialdehyde production by platelets during secondary aggregation.

A method is described for increasing the sensitivity of the thiobarbiturate assay for malondialdehyde by concentrating the coloured reaction product. The basal level of malondialdehyde-like material in plasma was found to be about 0.03 micrometer. Platelets synthesized malondialdehyde when stimulated by collagen or thrombin and also during the second phase of aggregation induced by ADP or adrenaline.

Adenosine Diphosphate↗
PubMed1979

Ageing of Neurospora crassa. VIII. Lethality and mutagenicity of ferrous ions, ascorbic acid, and malondialdehyde.

Ferrous ions were highly lethal and mutagenic to germinated conidia of Neurospora crassa. At comparable survival, treatment with 0.2 mM ferrous ions was 14- and 50-fold more mutagenic than ultra-violet irradiation or X-rays, respectively, in the reversion of an inositol auxotroph. Ascorbic acid alone (2 mM) was not reproducibly lethal and inhibited both the lethality and mutagenicity of ferrous ions. Bovine superoxide dismutase (SOD) completely inhibited the residual lethality of ferrous ascorbate. Protection by ascorbic acid and SOD indicates that superoxide radicals, generated by oxidation of Fe(II), are directly or indirectly mutagenic and lethal. Malondialdehyde (MDA) was lethal and appeared to be mutagenic; however, its action is probably different from that of superoxide. Therefore, superoxide-mediated production of endogenous MDA by way of peroxidation of polyunsaturated fatty acids is probably not an alternate mutagenic pathway, at least in the reversion of the allele of the inl locus examined. These results and the demonstration of superoxide-mediated decrease in the synthetic fidelity of DNA polymerase in vitro (Rana and Munkres, in preparation) warrant additional exploration of the hypothesis that endogenous cellular free radicals, generated by pre- and post-senescent metabolism, may enter into lethal and mutagenic reactions.

Aging↗
PubMed1979

Platelet aggreation malondialdehyde formation in type IIA hypercholesterolemic patients.

Platelet aggregation induced by threshold concentrations of ADP, adrenaline, collagen and Thrombofax was evaluated in 25 type IIA hypercholesterolemic patients in comparison with 15 control subjects. Malondialdehyde (MDA) formation induced by collagen and thrombin was also studied in a subgroup of 8 patients. In the patient group, irreversible platelet aggregation was induced by significantly lower concentrations of both adrenaline (p is less than 0.05) and Thrombofax (p is less than 0.01). MDA formation induced by both aggregating agents was markedly increased (p is less than 0.01) in type IIA hypercholesterolemic patients.

Adult↗
PubMed1992

Inhibitory effect of aryl thienyl-ketones and -thioketones on arachidonic acid-induced malondialdehyde formation in human platelets: biological data and molecular modelling.

A series of anti-thrombotic aryl thienyl-ketones and -thioketones was assayed in vitro for their inhibitory effect on malondialdehyde (MDA) production induced by arachidonic acid in human platelets. For several compounds MDA formation was strongly inhibited indicating that the anti-platelet target was situated on the cyclooxygenase pathway. A comparison between the inhibition constant Ki and the IC50 values revealed competitive inhibition kinetics. The molecular structure of one active compound was analysed by X-ray diffraction and theoretical calculations to provide information on its electronic and lipophilic properties.

Arachidonic Acid↗
PubMed1979

[Effect of factor VIII concentrate on malondialdehyde release by normal human platelets].

It is well known that Factor VIII concentrates affect platelet function both "in vitro" and "in vivo" but the mechanism of their action is poorly understood. Therefore the aim of the present work was to investigate a possible effect of these concentrates on prostaglandin synthesis by platelets, measured as the amount of released malondialdehyde (MDA), which is an index of Thromboxane A2 production. Our data suggest that Factor VIII concentrates have no effect on MDA release by platelets and on its inhibition by aspirin and heparin. In conclusion the effect of Factor VIII concentrates on platelets is not mediated by an increased synthesis of prostaglandins.

Adult↗
PubMed1992

Platelet levels of reduced glutathione, superoxide dismutase, zinc and malondialdehyde in uremic patients.

Platelet-reduced glutathione (GSH), superoxide dismutase (SOD) and zinc content as well as malondialdehyde (MDA) formation were studied in 24 healthy volunteers as controls and 25 patients with chronic renal failure. Uremic patients had a significantly lower GSH and SOD content as well as an abnormal MDA formation in platelets. Their plasma zinc levels were sharply below the normal value, but the platelet zinc content was similar to normal controls. The decrease in the platelet GSH level was closely related to plasma zinc in uremic patients. We also found that the platelet zinc levels were positively correlated to the platelet GSH content in normal controls and uremic patients, but not to the platelet SOD level. The results suggest that uremic toxins may influence the content of platelet GSH and SOD, as well as inhibit prostaglandin synthesis. The decreases in platelet GSH may partially be related to the low plasma zinc level.

Adult↗
PubMedDate not supplied

Ascorbic acid did not alter the content of conjugated dienes and malondialdehyde in organs of mice.

The aim of this study was to explore whether ip administration of ascorbic acid (AA) in a dose of 500 mg/kg, once a day for 3 following days, affected the content of lipid peroxidation products: malondialdehyde (MDA) and conjugated dienes (CD) in organs of mice. Injection of AA caused 2.1-, 1.3- and 1.8-fold increase in the concentration of this vitamin in liver, spleen and lungs, respectively, while the content of MDA and CD in these organs did not differ from values found in animals treated with 0.9% NaCl. It suggests that in our animal model AA did not act as a prooxidant enhancing the lipid peroxidation in various tissues.

Animals↗
PubMed1979

Influence on thromboxane and malondialdehyde synthesis in human thrombocytes by various inhibitors of platelet function.

The effects of various inhibitors of platelet function have been compared with respect to the minimal effective concentration required to inhibit platelet aggregation and the thromboxane (TXA2) and malondialdehyde (MDA) synthesis in washed platelets. The potencies of the agents in the different platelet function tests showed no consistent correlation. The most striking difference was found between the prostaglandins and the adenine nucleotides. The prostaglandins PGE1 and PGI2 inhibited all platelet reactions (10(-7) - 10(-8) g/ml) which may be explained by their stimulation of adenylcyclase. In contrast, the adenine nucleotides adenosine and AMP which are supposed to raise cAMP platelets via the same mechanism and strongly inhibited primary and secondary platelet aggregation (3 x 10(-6) - 3 x 10(-7) g/ml) had no effect on TXA2 and MDA synthesis. The results suggest that the pharmacological inhibition of platelet function may not act via a uniform mechanism controlled by the arachidonate pathway.

Adenine Nucleotides↗