scholarly journals Low-density lipoprotein mimics blood plasma-derived exosomes and microvesicles during isolation and detection

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Barbara W Sódar ◽  
Ágnes Kittel ◽  
Krisztina Pálóczi ◽  
Krisztina V Vukman ◽  
Xabier Osteikoetxea ◽  
...  
2021 ◽  
Vol 3 (1) ◽  
pp. 104-109
Author(s):  
Yola Noveraz Nasa ◽  
Nugraha Sutadipura ◽  
Santun Bhekti Rahimah

Konsumsi bensin sejak tahun 2000 sampai 2014 meningkat seiring dengan peningkatan jumlah kendaraan bermotor setiap tahun. Bensin memiliki dampak negatif terhadap lingkungan berupa polusi dan terhadap kesehatan seperti gangguan paru, ginjal, penyakit kulit, serta perubahan profil lipid berupa peningkatan kadar low-density lipoprotein (LDL) yang dapat meningkatkan angka kejadian penyakit jantung koroner dan sindrom metabolik. Tujuan penelitian mengetahui pengaruh paparan bensin terhadap kadar LDL pada plasma darah manusia yang dimulai dengan kajian terhadap hewan coba. Metode penelitian yang digunakan yaitu deskriptif dengan prosedur scoping review dengan cara mengidentifikasi, menganalisis dan mengevaluasi karya ilmiah sesuai dengan kriteria inklusi dan eksklusi serta diskrining menggunakan kriteria kelayakan (Eligibility criteria). Hasil penelitian didapatkan sepuluh artikel dari jumlah awal 10.486 artikel yang ditemukan dari kata kunci. Sepuluh artikel yang sesuai dengan PICO (Population: tikus; Intervention: bensin, lead atau benzene;  Comparison: tikus yang tidak dipaparkan bensin, lead atau benzene; Outcome: kadar LDL pada plasma darah) menunjukkan peningkatan kadar LDL plasma pada kelompok tikus yang diberi paparan bensin, timbal atau benzena daripada kelompok kontrol. Hal tersebut diakibatkan stres oksidatif dari induksi lead atau benzene yang menekan aktivitas antioksidan dan meningkatkan reactive oxygen species di tubuh sehingga terjadi cidera hepar dan metabolisme lipoproteinpun terganggu. Pada akhirnya bensin yang memiliki komponen benzene atau lead mengakibatkan peningkatan kadar LDL plasma. Kesimpulan penelitian terdapat pengaruh bensin terhadap kadar LDL pada plasma darah tikus dan beberapa komponen bensin yang berperan, yaitu timbal dan benzena. Scoping Review: Effect of Gasoline on Increasing Blood Plasma LDL Levels in Rats Gasoline consumption from 2000 to 2014 increased along with the increase in the number of motorized vehicles each year. Gasoline harms the environment in the form of pollution and on the health of lung, kidney, skin diseases, and changes in the lipid profile in the form of increased levels of low-density lipoprotein (LDL) which can increase the incidence of coronary and metabolic heart disease. This study aimed to determine the effect of gasoline exposure on LDL levels in human blood plasma starting with a study of experimental animals. The research method used is descriptive with a scoping review procedure by identifying, analyzing, and evaluating scientific papers according to inclusion and exclusion criteria and screening using eligibility criteria. The research results obtained ten articles from the initial number of 10,486 articles found from keywords. Ten PICO-compliant articles (Population: rats; Intervention: gasoline, lead or benzene; Comparison: rats not exposed to gasoline, lead or benzene; Results: LDL levels in blood plasma) showed increased plasma LDL levels in the group of rats exposed to gasoline, lead or benzene control group. This is due to oxidative stress from lead or benzene induction which suppresses antioxidant activity and increases reactive oxygen species in the body, resulting in liver injury, impaired lipoprotein metabolism. In the end, gasoline which has benzene or lead component causes an increase in plasma LDL levels. This study concludes that there is an effect of gasoline on LDL levels in rat blood plasma, and several components of gasoline that play a role, namely lead and benzene.


2018 ◽  
Vol 90 (9) ◽  
pp. 27-30 ◽  
Author(s):  
V Z Lankin ◽  
A K Tikhaze ◽  
M Viigimaa ◽  
I E Chazova

Aim. We study the dynamics of oxidatively modified low-density lipoprotein (ox-LDL) content in blood plasma, as well as changes in the activity of key antioxidant enzymes such as Se-containing glutathione peroxidase (GSH-Px) Cu,Zn-superoxide dismutase (SOD) and catalase in erythrocytes of patients with coronary artery disease during treatment with PCSK9 inhibitor (ewolocumab). Materials and methods. The study included 9 men (59 ± 10 years) with coronary artery disease with atherosclerotic lesion at least one main coronary artery according to coronary angiography. Patients took standard therapy before taking the study, everyone took the maximum tolerated dose of statins. Since the target cholesterol levels of low-density lipoprotein cholesterol (LDL-C) were not achieved during the statin therapy, patients were prescribed lipid-lowering therapy with the inclusion of the inhibitor PCSK9-emocoucumab from Amgen 420 mg once a month. The content of lipid metabolism indices was determined by standard biochemical methods. The level of ox-LDL in the blood plasma was determined by the immunochemical method. The activity of antioxidant enzymes was determined in blood erythrocytes using biochemical techniques Results. Cholesterol-lowering drug of the new type - inhibitor protein convertase subtilisin/kexin type 9 (PCSK9) evolocumab (Amgen) not only effectively lowers the level of cholesterol in low density lipoprotein (LDL), but also significantly reduces the content of oxdatively modified LDL in blood plasma. Unlike statins, the inhibitor of PCSK9 does not cause a decrease in the activity of antioxidant enzymes of the blood. Conclusion. PCSK9 inhibitor has no effect on the parameters of oxidative stress.


1995 ◽  
Vol 50 (9-10) ◽  
pp. 699-707 ◽  
Author(s):  
Elke Schlüssel ◽  
Gudrun Preibisch ◽  
S. Piitter ◽  
E. F. Elstner

Abstract Increased blood plasma concentrations of the sulphur amino acid homocysteine (“homocysteinemia”) have been brought into context with neurodegenerative and arteriosclerotic symptoms and diseases. We recently reported on biochemical model reactions on the prooxidative activity of hom ocysteine including the desactivation of Na+/K+-ATPases and hemolysis of erythrocytes (Preibisch et al., 1993). In this communication we extend our model reactions including the oxidation of methionine, metabolization of pyridoxalphosphate and dihydroxyphenylalanine, desactivations of transaminases and peroxidation of low density lipoprotein


Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 363 ◽  
Author(s):  
Karsten-H. Weylandt ◽  
Christoph Schmöcker ◽  
Annika I. Ostermann ◽  
Laura Kutzner ◽  
Ina Willenberg ◽  
...  

Lipoprotein apheresis reliably reduces low-density lipoprotein (LDL) cholesterol in patients with atherosclerotic disease and therapy-refractory hypercholesterolemia or elevated lipoprotein (a) (Lp(a)). Besides lowering lipoproteins and triglycerides, apheresis also decreases levels of essential omega-6 and omega-3 polyunsaturated fatty acids (n-6 and n-3 PUFAs) in blood plasma. In contrast, heparin-induced extracorporeal low-density lipoprotein precipitation (HELP) lipid apheresis might increase the formation of potentially pro-inflammatory and pro-thrombotic lipid mediators derived from n-6 and n-3 PUFAs. The study presented here analyzed lipid mediator profiles in the plasma of patients with hyperlipidemia treated by one of three different apheresis methods, either HELP, direct absorption (DA), or membrane filtration (MDF), in a direct pre- and post-apheresis comparison. Using gas chromatography and liquid chromatography tandem mass spectrometry (LC-MS/MS) we were able to analyze fatty acid composition and the formation of lipid mediators called oxylipins. Our data illustrate—particularly in HELP-treated patients—significant decreases of essential omega-6 and omega-3 polyunsaturated fatty acids in blood plasma but significant increases of PUFA-derived lipoxygenase-, as well as cyclooxygenase- and cytochrome P450-derived lipid mediators. Given that n-3 PUFAs in particular are presumed to be cardioprotective and n-3 PUFA-derived lipid mediators might limit inflammatory reactions, these data indicate that n-3 PUFA supplementation in the context of lipid apheresis treatment might have additional benefits through apheresis-triggered protective n-3 PUFA-derived lipid mediators.


2016 ◽  
Vol 62 (4) ◽  
pp. 391-402 ◽  
Author(s):  
V.N. Sukhorukov ◽  
V.P. Karagodin ◽  
A.N. Orekhov

One of the first manifestations of atherosclerosis is accumulation of extra- and intracellular cholesterol esters in the arterial intima. Formation of foam cells is considered as a trigger in the pathogenesis of atherosclerosis. Low density lipoprotein (LDL) circulating in human blood is the source of lipids accumulated in the arterial walls. This review considered features and role in atherogenesis different modified forms of LDL: oxidized, small dense, electronegative and especially desialylated LDL. Desialylated LDL of human blood plasma is capable to induce lipid accumulation in cultured cells and it is atherogenic. LDL possesses numerous alterations of protein, carbohydrate and lipid moieties and therefore can be termed multiple-modified LDL. Multiple modification of LDL occurs in human blood plasma and represents a cascade of successive changes in the lipoprotein particle: desialylation, loss of lipids, reduction in the particle size, increase of surface electronegative charge, etc. In addition to intracellular lipid accumulation, stimulatory effects of naturally occurring multiple-modified LDL on other processes involved in the development of atherosclerotic lesions, namely cell proliferation and fibrosis, were shown.


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