Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages

Glutaraldehyde treatment of 125I-labeled density compound protein (125I-native-LDL) created a changed lipoprotein (125I-glut-LDL) with a relative molecular mass of ten × 106 or a lot of. Malondialdehyde treatment of 125I-native-LDL created a product (125I-MDA-LDL) with a relative molecular mass not appreciably totally different from that of the first compound protein. However, the activity quality of MDA-LDL indicated a a lot of electric charge than native-LDL. 125I-MDA-LDL was degraded by 2 methodes: a high-affinity saturable process with greatest speed at 10-15 μg of supermolecule per mil and a slower, nonsaturable method. The degradation of 125I-MDA-LDL was pronto restrained by increasing concentrations of nonradioactive MDA-LDL however wasn’t restrained by acetylated lipoprotein or native-LDL even at concentrations as high as 1600 μg of supermolecule per mil. when exposure of native-LDL to protoplasm aggregation and unleash in vitro, 1.73 ± 0.19 nmol of malondialdehyde per mg of lipoprotein supermolecule was certain to the platelet-modified-LDL. No detectable malondialdehyde was recovered from native-LDL that had been treated identically except that the platelets were omitted from the reaction mixture.

After incubation with glut-LDL, MDA-LDL, or platelet-modified-LDL for three days, human monocyte-macrophages showed a dramatic increase in cholesteryl organic compound content whereas the cholesteryl organic compound content of cells incubated with a similar concentration of native-LDL failed to. supported these experiments we tend to propose that modification of native-LDL is also a necessity to the buildup of cholesteryl esters at intervals the cells of the induration of the arteries reaction. we tend to any expect that one modification of lipoprotein in vivo could result from malondialdehyde that is free from blood platelets or is created by lipoid peroxidation at the location of blood vessel injury. [1]

Malondialdehyde-altered protein occurs in atheroma of Watanabe heritable hyperlipidemic rabbits

It has been planned that with chemicals reactive supermolecules free throughout lipid peroxidation convert density conjugated protein (LDL), the foremost carrier of plasma sterol, to associate degree abnormal kind which receptor-mediated clearance of this altered lipoprotein produces cholesteryl organic compound deposition in macrophage-derived foam cells of fatty tissue. Immuno-cytochemical analyses currently reveal the presence of macromolecule changed by malondialdehyde, a peroxidative effect, that colocalizes with the living thing deposition of apolipoprotein B-100 macromolecule of lipoprotein in fatty tissue from Watanabe transmitted hyperlipidemic rabbits. These findings give evidence for the existence in vivo of macromolecule changed by a physiological product of supermolecule peroxidation among blood vessel lesions. [2]

Malondialdehyde formation as an indicator of prostaglandin production by human platelets

The formation of malondialdehyde, a substance of autacoid endoperoxides, has been studied in platelet-rich plasma. tiny amounts were made in response to ADP, hormone, or albuminoid and bigger amounts in response to coagulase. Arachidonic acid induced  platelets to supply giant amounts of malondialdehyde. Malondialdehyde formation by platelets was prevented by pain pill or Indocin. The measure of malondialdehyde in living substance-rich plasma could also be used as Associate in Nursing indicator of platelet autacoid synthesis, and is less complicated than the measure of prostaglandins. [3]

Effect of mode of birth on purine and malondialdehyde in umbilical arterial plasma in normal term newborns

Objective: to look at the impact of mode of birth on plasma purine and malondialdehyde levels in traditional term infants.

Study Design: point blood vessel wire blood was obtained at once when birth from a convenience sample of 119 traditional term newborns born by duct delivery, with or while not internal secretion augmentation or by elective cesarian. Plasma was analyzed for purine and/or malondialdehyde levels. Numeric information were analyzed utilizing freelance samples t-test and ordinal data were analyzed victimisation Mann–Whitney check. Correlation coefficients were obtained victimisation Spearman’s ρ.

Result: acid levels were considerably elevated.  [4]

Evaluation of Insulin, Malondialdehyde and Blood Pressure in Male Obese Individuals in Nnewi and Subsequent Effect of Green Tea Supplementation

Background: fleshiness could be a major public health issue worldwide, contributive to raised vessel diseases, diabetes, endocrine resistance and aerobic  stress. this is often because of inactive lifestyles; poor fasting and low consumption of inhibitor supplement (example inexperienced tea). the target of this study was to guage the amount of fast glucose, insulin, endocrine resistance vital sign and MDA in rotund subjects and succeeding impact of tea at 6weeks and 12weeks supplementation.

Methods: This was a cross sectional and interventional study. within the cross sectional study, eighty eight rotund subjects (46 category I and forty two category II obese) and fifty traditional weight subjects (control) were recruited. within the interventional study, twenty male rotund subjects were indiscriminately selected  and got 200ml of commercially ready tea. fast blood samples were collected before the intervention (baseline), at 6weeks and 12weeks of intervention and were later analyzed by normal technique accelerator connected bioassay and colorimeteric technique. it had been analysed statistically exploitation SPSS version twenty three.0.

Results: there have been vital will increase within the mean levels of HOMA-IR, pulse and heartbeat blood pressures, fast plasma aldohexose and endocrine in rotund subjects (class II and sophistication I obese) when put next with management cluster. [5]

Reference

[1] Fogelman, A.M., Shechter, I., Seager, J., Hokom, M., Child, J.S. and Edwards, P.A., 1980. Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages. Proceedings of the National Academy of Sciences, 77(4), pp.2214-2218. (Web Link)

[2] Haberland, M.E., Fong, D. and Cheng, L., 1988. Malondialdehyde-altered protein occurs in atheroma of Watanabe heritable hyperlipidemic rabbits. Science, 241(4862), pp.215-218. (Web Link)

[3] Smith, J.B., Ingerman, C.M. and Silver, M.J., 1976. Malondialdehyde formation as an indicator of prostaglandin production by human platelets. The Journal of laboratory and clinical medicine, 88(1), pp.167-172. (Web Link)

[4] Effect of mode of birth on purine and malondialdehyde in umbilical arterial plasma in normal term newborns

T C Calderon, W Wu, R A Rawson, E P Sakala, L C Sowers, D S Boskovic & D M Angeles

Journal of Perinatology volume 28, pages 475–481 (2008) (Web Link)

[5] Samuel Chukwuemeka, M., Ifeoma Joy, O., Chudi Emmanuel, D., Chikaodili Nwando, O.-E. and Saheed Opeyemi, U. (2018) “Evaluation of Insulin, Malondialdehyde and Blood Pressure in Male Obese Individuals in Nnewi and Subsequent Effect of Green Tea Supplementation”, Asian Journal of Research in Medical and Pharmaceutical Sciences, 3(3), pp. 1-7. doi: 10.9734/AJRIMPS/2018/41153. (Web Link)

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