Augmenter of liver regeneration (ALR) contributes to mitochondrial biogenesis, maintenance and to the physiological operation of mitochondria. The depletion of ALR has been widely studied and had serious consequences on the mitochondrial functions. However the inverse direction, the effect of the depletion of mitochondrial electron transfer chain and mtDNA on ALR expression has not been investigated yet. Thus mtDNA depleted, ρ(0) cell line was prepared to investigate the role of mitochondrial electron transfer chain and mtDNA on ALR expression. The depletion of mtDNA has not caused any difference at mRNA level, but at protein level the expression of ALR has been markedly increased. The regulatory role of ATP and ROS levels could be ruled out because the treatment of the parental cell line with different respiratory inhibitors and uncoupling agent could not provoke any changes in the protein level of ALR. The effect of mtDNA depletion on the protein level of ALR has been proved not to be liver specific, since the phenomenon could be observed in the case of two other, non-hepatic cell lines. It seems the level of mtDNA and/or its products may have regulatory role on the protein level of ALR. The up-regulation of ALR can be a part of the adaptive response in ρ(0) cells that preserves the structural integrity and the transmembrane potential despite the absence of protein components encoded by the mtDNA.
Although vitamin C is essential as an antioxidant and as a cofactor in a series of enzymatic reactions, the ability for ascorbate biosynthesis was lost in humans. Thus, horticultural products and derived fruit drinks or commercial vitamin C products are considered to be important sources for the ascorbic acid intake in the human diet. These facts underline the importance of analytical methods for ascorbic acid determination in different food products.In our study two spectrophotometric and a fl uorometric ascorbic acid determination methods have been compared with each other and with the so-called etalon HPLC method to fi nd the best for small or middle sized food analytic laboratories with a sample number of up to several hundreds. As a result of our experiments we could establish that the OPDA-fl uorometric method can be suggested for the determination of samples containing ascorbate at low concentrations. Unfortunately, the analytical properties of the OPDA method with spectrophotometric detection have been lagging far behind the others. The 2,2'-bipyridyl method could give a balanced performance for all tests. Furthermore, the results gained by this method are the closest to the results of the reference HPLC method in the case of fruit and vegetable samples.
Az ALR fehérje egy igazi misztikum. A fehérje egy hosszabb, 22 kDa-os és egy rövidebb, 15 kDa-os formában léte-zik. A hetvenes években részleges hepatectomián átesett állatokban fedezték fel és kizárólag a májregeneráció egyik kulcsfehérjéjének tartották. A 2000-es évek elején kiderült, hogy a "hosszú" forma a mitokondriális intermembrán terében lokalizálódik és kisméretű fehérjék mitokondriális importjának és oxidatív foldingjának kapcsolt folyamatá-ban vesz részt. A rendszer szubsztrátjai között több, alapvető mitokondriális folyamatokban nélkülözhetetlen fehérje megtalálható, ezért az ALR génjében bekövetkező mutációk mitokondriális rendellenességekhez vezethetnek. Az ALR "rövid" formája az emlősök szervezetében szekretált extracelluláris növekedési faktorként funkcionál, és változatos módokon képes elősegíteni a hepatocyták védelmét, regenerációját és proliferációját. A közelmúltban elő-állított kondicionális ALR-mutáns egereken nyert eredmények arra utalnak, hogy fontos szerepet kaphat az alkoholos és nem alkoholos steatosis kialakulásában is. Tekintve, hogy számos, májat érintő elváltozás során megváltozik szé-rumszintje, ígéretes markermolekula-jelölt a laboratóriumi diagnosztikában. Orv. Hetil., 2015, 156(13), 503-509.Kulcsszavak: ALR, máj, oxidatív folding, mitokondrium, steatosis ALR, the multifunctional protein ALR is a mystic protein. It has a so called "long" 22 kDa and a "short" 15 kDa forms. It has been described after partial hepatectomy and it has just been considered as a key protein of liver regeneration. At the beginning of the 21 st century it has been revealed that the "long" form is localized in the mitochondrial intermembrane space and it is an element of the mitochondrial protein import and disulphide relay system. Several proteins of the substrates of the mitochondrial disulphide relay system are necessary for the proper function of the mitochondria, thus any mutation of the ALR gene leads to mitochondrial diseases. The "short" form of ALR functions as a secreted extracellular growth factor and it promotes the protection, regeneration and proliferation of hepatocytes. The results gained on the recently generated conditional ALR mutant mice suggest that ALR can play an important role in the pathogenesis of alcoholic and non-alcoholic steatosis. Since the serum level of ALR is modifi ed in several liver diseases it can be a promising marker molecule in laboratory diagnostics. ÖSSZEFOGLALÓ KÖZLEMÉNYRövidítések ALR = augmenter of liver regeneration; ALT = alanin-aminotranszferáz; AP1 = aktivátor protein 1; ATP = adenozin-trifoszfát; EGF = epidermal growth factor; EGFR = epidermal growth factor receptor; ERK1/2 = extracellular signal-regulated kinase 1/2; ERV1/2 = essential for respiration and viability 1/2; GFER = growth factor ERV1 homolog; HGF = hepatocyte growth factor; HSS = hepatocyte stimulator substance; IL-1/6 = interleukin-1/6; IMS = mitokondriális intermembrán tér; JAB1 = Jun-activating domain-binding protein 1; LPS = lipopoliszacharid; MAPK = mitogen-activated protein kinase; MI...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.