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Article ; Online: The interlacing anticancer effect of pharmacologic ascorbate, chloroquine, and resveratrol.

Makk-Merczel, Kinga / Varga, Dóra / Hajdinák, Péter / Szarka, András

2024

Abstract: Currently, a diagnosis with KRAS mutant pancreatic ductal adenocarcinoma (PDAC) means a death warrant, so finding efficient therapeutic options is a pressing issue. Here, we presented that pharmacologic ascorbate, chloroquine and resveratrol co-treatment ...

Abstract	Currently, a diagnosis with KRAS mutant pancreatic ductal adenocarcinoma (PDAC) means a death warrant, so finding efficient therapeutic options is a pressing issue. Here, we presented that pharmacologic ascorbate, chloroquine and resveratrol co-treatment exerted a synergistic cytotoxic effect on PDAC cell lines. The observed synergistic cytotoxicity was a general feature in all investigated cancer cell lines independent of the KRAS mutational status and seems to be independent of the autophagy inhibitory effect of chloroquine. Furthermore, it seems that apoptosis and necroptosis are also not likely to play any role in the cytotoxicity of chloroquine. Both pharmacologic ascorbate and resveratrol caused double-strand DNA breaks accompanied by cell cycle arrest. It seems resveratrol-induced cytotoxicity is independent of reactive oxygen species (ROS) generation and accompanied by a significant elevation of caspase-3/7 activity, while pharmacologic ascorbate-induced cytotoxicity shows strong ROS dependence but proved to be caspase-independent. Our results are particularly important since ascorbate and resveratrol are natural compounds without significant harmful effects on normal cells, and chloroquine is a known antimalarial drug that can easily be repurposed.
Language	English
Publishing date	2024-03-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	59230-4
ISSN	1872-8081 ; 0951-6433
ISSN (online)	1872-8081
ISSN	0951-6433
DOI	10.1002/biof.2050
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Article: A β-AMILOID ÉS A MITOCHONDRIALIS DISZFUNKCIÓ SZEREPE AZ ALZHEIMER-KÓR PATOGENEZISÉBEN.

Szarka, András

Ideggyogyaszati szemle

2015 Volume 68, Issue 7-8, Page(s) 222–228

Abstract: Alzheimer's disease is the most common form of dementia in mid- and late life. The 7-10% of the population over 65 and the 50-60% of the population over 85 are affected by this disease. In spite of its prevalence, the pathogenesis of the disease is not ... ...

Title translation	THE ROLE OF β-AMYLOID AND MITOCHONDRIAL DYSFUNCTION IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE.
Abstract	Alzheimer's disease is the most common form of dementia in mid- and late life. The 7-10% of the population over 65 and the 50-60% of the population over 85 are affected by this disease. In spite of its prevalence, the pathogenesis of the disease is not well defined and there is no effective neuroprotective therapeutic agent. Three predominant neuropathologic features of the brain in Alzheimer disease are: the intracellular neurofibrillary tangles consisting mainly of the hyperphosphorylated protein τ; the extracellular amyloid deposits (neuritic plaques) consisting of amyloid β peptide; and the extensive neuronal cell loss in the hippocampus and in portions of the cerebral cortex. The possible reason of the extensive neuronal cell loss can be the mitochondrial dysfunction observed in Alzheimer's disease. Beyond the uncertain pathogenesis, the causality of these characteristic neuropathologic phenomena are still unknown. In this study we present two hypotheses, one of the amyloid cascade and one of the mitochondrial cascade. We give an overview of these two hypotheses and discuss their correlations.
MeSH term(s)	Aging ; Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Brain/pathology ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Hippocampus/metabolism ; Hippocampus/pathology ; Humans ; Mitochondria/metabolism ; Neurofibrillary Tangles/metabolism ; Neurons/pathology ; Oxidative Stress ; Prevalence ; Signal Transduction
Chemical Substances	Amyloid beta-Peptides
Language	Hungarian
Publishing date	2015-09-08
Publishing country	Hungary
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	2240317-6
ISSN	0019-1442
ISSN	0019-1442
DOI	10.18071/isz.68.0222
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Article ; Online: Friend or Foe: The Relativity of (Anti)oxidative Agents and Pathways.

Szarka, András / Lőrincz, Tamás / Hajdinák, Péter

International journal of molecular sciences

2022 Volume 23, Issue 9

Abstract: An element, iron, a process, the generation of reactive oxygen species (ROS), and a molecule, ascorbate, were chosen in our study to show their dual functions and their role in cell fate decision. Iron is a critical component of numerous proteins ... ...

Abstract	An element, iron, a process, the generation of reactive oxygen species (ROS), and a molecule, ascorbate, were chosen in our study to show their dual functions and their role in cell fate decision. Iron is a critical component of numerous proteins involved in metabolism and detoxification. On the other hand, excessive amounts of free iron in the presence of oxygen can promote the production of potentially toxic ROS. They can result in persistent oxidative stress, which in turn can lead to damage and cell death. At the same time, ROS-at strictly regulated levels-are essential to maintaining the redox homeostasis, and they are engaged in many cellular signaling pathways, so their total elimination is not expedient. Ascorbate establishes a special link between ROS generation/elimination and cell death. At low concentrations, it behaves as an excellent antioxidant and has an important role in ROS elimination. However, at high concentrations, in the presence of transition metals such as iron, it drives the generation of ROS. In the term of the dual function of these molecules and oxidative stress, ascorbate/ROS-driven cell deaths are not necessarily harmful processes-they can be live-savers too.
MeSH term(s)	Antioxidants/metabolism ; Iron/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/metabolism
Chemical Substances	Antioxidants ; Reactive Oxygen Species ; Iron (E1UOL152H7)
Language	English
Publishing date	2022-05-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23095188
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Article ; Online: The Possible Connection of Two Dual Function Processes: The Relationship of Ferroptosis and the JNK Pathway.

Varga, Dóra / Hajdinák, Péter / Makk-Merczel, Kinga / Szarka, András

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Ferroptosis represents a typical process that has dual functions in cell fate decisions since the reduction and/or inhibition of ferroptosis is desirable for the therapies of diseases such as neurological disorders, localized ischemia-reperfusion, kidney ...

Abstract	Ferroptosis represents a typical process that has dual functions in cell fate decisions since the reduction and/or inhibition of ferroptosis is desirable for the therapies of diseases such as neurological disorders, localized ischemia-reperfusion, kidney injury, and hematological diseases, while the enhanced ferroptosis of cancer cells may benefit patients with cancer. The JNK pathway also has a real dual function in the fate of cells. Multiple factors suggest a potential link between the ferroptotic and JNK pathways; (i) both processes are ROS mediated; (ii) both can be inhibited by lipid peroxide scavengers; (iii) RAS mutations may play a role in the initiation of both pathways. We aimed to investigate the possible link between ferroptosis and the JNK pathway. Interestingly, JNK inhibitor co-treatment could enhance the cancer cytotoxic effect of the ferroptosis inducers in NRAS and KRAS mutation-harboring cells (HT-1080 and MIA PaCa-2). Since cancer's cytotoxic effect from the JNK inhibitors could only be suspended by the ferroptosis inhibitors, and that sole JNK-inhibitor treatment did not affect cell viability, it seems that the JNK inhibitors "just" amplify the effect of the ferroptosis inducers. This cancer cell death amplifying effect of the JNK inhibitors could not be observed in other oxidative stress-driven cell deaths. Hence, it seems it is specific to ferroptosis. Finally, our results suggest that GSH content/depletion could be an important candidate for switching the anti-cancer effect of JNK inhibitors.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Ferroptosis ; Humans ; Lipid Peroxides ; MAP Kinase Signaling System ; Neoplasms/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Antineoplastic Agents ; Lipid Peroxides ; Reactive Oxygen Species ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2022-09-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231911004
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Article ; Online: Therapeutic Approach of KRAS Mutant Tumours by the Combination of Pharmacologic Ascorbate and Chloroquine.

Kapuy, Orsolya / Makk-Merczel, Kinga / Szarka, András

Biomolecules

2021 Volume 11, Issue 5

Abstract: The Warburg effect has been considered a potential therapeutic target to fight against cancer progression. In KRAS mutant cells, PKM2 (pyruvate kinase isozyme M2) is hyper-activated, and it induces GLUT1 expression; therefore, KRAS has been closely ... ...

Abstract	The Warburg effect has been considered a potential therapeutic target to fight against cancer progression. In KRAS mutant cells, PKM2 (pyruvate kinase isozyme M2) is hyper-activated, and it induces GLUT1 expression; therefore, KRAS has been closely involved in the initiation of Warburg metabolism. Although mTOR (mammalian target of rapamycin), a well-known inhibitor of autophagy-dependent survival in physiological conditions, is also activated in KRAS mutants, many recent studies have revealed that autophagy becomes hyper-active in KRAS mutant cancer cells. In the present study, a mathematical model was built containing the main elements of the regulatory network in KRAS mutant cancer cells to explore the further possible therapeutic strategies. Our dynamical analysis suggests that the downregulation of KRAS, mTOR and autophagy are crucial in anti-cancer therapy. PKM2 has been assumed to be the key switch in the stress response mechanism. We predicted that the addition of both pharmacologic ascorbate and chloroquine is able to block both KRAS and mTOR pathways: in this case, no GLUT1 expression is observed, meanwhile autophagy, essential for KRAS mutant cancer cells, is blocked. Corresponding to our system biological analysis, this combined pharmacologic ascorbate and chloroquine treatment in KRAS mutant cancers might be a therapeutic approach in anti-cancer therapies.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Chloroquine/pharmacology ; Models, Theoretical ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Pyruvate Kinase/drug effects ; Pyruvate Kinase/metabolism ; Signal Transduction/drug effects ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases/metabolism ; Warburg Effect, Oncologic/drug effects
Chemical Substances	Antineoplastic Agents ; KRAS protein, human ; Chloroquine (886U3H6UFF) ; Pyruvate Kinase (EC 2.7.1.40) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2021-04-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom11050652
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Article ; Online: A karbonilstressz szerepe a diabetes szövődményeinek kialakulásában.

Makk-Merczel, Kinga / Szarka, András

Orvosi hetilap

2018 Volume 160, Issue 40, Page(s) 1567–1573

Abstract: The relationship between the potentially developing complications of the 451 million people affected by diabetes and hyperglycaemia can be based on the enhanced generation of advanced glycation endproducts and the more intensive oxidative and carbonyl ... ...

Title translation	The role of carbonyl stress in the development of diabetic complications.
Abstract	The relationship between the potentially developing complications of the 451 million people affected by diabetes and hyperglycaemia can be based on the enhanced generation of advanced glycation endproducts and the more intensive oxidative and carbonyl stress. Advanced glycation endproducts generated partly due to carbonyl stress play an important role in the pathogenesis of diabetic complications such as elevated arterial thickness, vascular permeability, enhanced angiogenesis or the more rigid vessels induced nephropathy, neuropathy, retinopathy. Furthermore, the elevated thrombocyte aggregation, the reduced fibrinolysis induced elevated coagulation, and the atherosclerosis or the mitochondrial dysfunction are important as well. The most potent target of both the non-oxidative and oxidative generation of advanced glycation endproducts can be the scavenging of α,β-unsaturated aldehydes. Although, aminoguanidine, the prototype of scavenger molecules, showed protection in different animal models, it failed in the human clinical studies. Finally, the clinical studies were terminated almost 20 years ago. The endogen dipeptide L-carnosine was also expected to mitigate the complications due to carbonyl stress. However, its clinical significance was limited by the serum carnosinases and by the consequent low serum stability and bioavailability. The carnosinase resistance of the molecule can be achieved by the change of the carboxyl group of the molecule to hydroxyl group. At the same time, the biosafety and the carbonyl stress scavenging activity of the molecule could be preserved. Although clinical studies could not be performed in the last six months, on the basis of the
MeSH term(s)	Animals ; Antioxidants/metabolism ; Diabetes Complications/metabolism ; Diabetes Complications/physiopathology ; Diabetes Mellitus ; Glycation End Products, Advanced/adverse effects ; Glycation End Products, Advanced/metabolism ; Glycation End Products, Advanced/physiology ; Humans ; Hyperglycemia ; Oxidative Stress/physiology
Chemical Substances	Antioxidants ; Glycation End Products, Advanced
Language	Hungarian
Publishing date	2018-06-18
Publishing country	Hungary
Document type	Journal Article ; Review
ZDB-ID	123879-6
ISSN	1788-6120 ; 0030-6002
ISSN (online)	1788-6120
ISSN	0030-6002
DOI	10.1556/650.2019.31519
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Article ; Online: Méhen belül felszívódó magzati mellékvesevérzés ultrahang-diagnózisa.

Szabó, Gábor / Szarka, András / Rudas, Gábor / Rigó, János

Orvosi hetilap

2020 Volume 160, Issue 52, Page(s) 2073–2078

Abstract: The confirmed incidence of new-onset adrenal gland hemorrhage has increased with the development of ultrasound diagnostics in recent years. Intrauterine developed cases are rarely recognized. Differential diagnosis of cystic lesions of the adrenal gland ... ...

Title translation	Ultrasound diagnosis of fetal adrenal hemorrhage.
Abstract	The confirmed incidence of new-onset adrenal gland hemorrhage has increased with the development of ultrasound diagnostics in recent years. Intrauterine developed cases are rarely recognized. Differential diagnosis of cystic lesions of the adrenal gland is often only possible after birth. In our case study, we report the ultrasonographic diagnosis and follow-up of a cystic lesion measuring 4 × 3 cm in the left fetal epigastrium in the 33rd gestational week. During pregnancy, multimodal imaging methods (both ultrasound and magnetic resonance) have confirmed the diagnosis of hemorrhage in the left adrenal gland. In the 37th gestational week, the hematoma completely resolved. At term, a 4150 gram neonate was delivered in good condition by an elective cesarean section. Postnatal endocrinological and follow-up ultrasound examinations did not find any disorder. This study is the first published case report in the literature that proves that fetal adrenal hemorrhage can intrauterin spontaneously absorb within a short period of time. Our case draws attention to the fact that adrenal bleeding may occur in the newborn regardless of birth trauma. It can also be assumed that the incidence of adrenal bleeding during pregnancy is higher than that reported in neonatal cases. Orv Hetil. 2019; 160(52): 2073-2078.
MeSH term(s)	Adrenal Gland Diseases/diagnosis ; Adrenal Gland Diseases/diagnostic imaging ; Adrenal Glands/diagnostic imaging ; Adrenal Glands/pathology ; Cesarean Section ; Diagnosis, Differential ; Female ; Fetal Diseases/diagnosis ; Hemorrhage/pathology ; Humans ; Infant, Newborn ; Pregnancy ; Ultrasonography, Prenatal/methods
Language	Hungarian
Publishing date	2020-01-03
Publishing country	Hungary
Document type	Journal Article
ZDB-ID	123879-6
ISSN	1788-6120 ; 0030-6002
ISSN (online)	1788-6120
ISSN	0030-6002
DOI	10.1556/650.2019.31578
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Article ; Online: Vitamin C and Cell Death.

Szarka, András / Kapuy, Orsolya / Lőrincz, Tamás / Bánhegyi, Gábor

Antioxidants & redox signaling

2020 Volume 34, Issue 11, Page(s) 831–844

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Apoptosis/drug effects ; Ascorbic Acid/therapeutic use ; Autophagy/drug effects ; Cell Death/drug effects ; Cell Death/genetics ; DNA Breaks, Double-Stranded/drug effects ; Ferroptosis/drug effects ; Humans ; Necroptosis/drug effects ; Neoplasms/diet therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Oxidative Stress/drug effects ; Poly (ADP-Ribose) Polymerase-1/genetics ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2020-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2019.7897
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Zs.A 5488: Show issues

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Article ; Online: The determination of hepatic glutathione at tissue and subcellular level.

Lőrincz, Tamás / Szarka, András

Journal of pharmacological and toxicological methods

2017 Volume 88, Issue Pt 1, Page(s) 32–39

Abstract: Introduction: Glutathione (GSH) through its important function in the antioxidant protection of cells and in the conjugation of drugs and xenobiotics has crucial importance in pharmacology and toxicology. Since GSH is most often measured in liver tissue ...

Abstract	Introduction: Glutathione (GSH) through its important function in the antioxidant protection of cells and in the conjugation of drugs and xenobiotics has crucial importance in pharmacology and toxicology. Since GSH is most often measured in liver tissue and different cell organelles it is important to choose the method that best suits for the determination of GSH. Methods: The GSH content of cell organelles isolated from control and BSO-treated liver tissues was determined by the GSH-NEM-HPLC-UV, monochlorobimane-GSH-HPLC-fluorescence method and DTNB-GSH recycling assay to find the most suitable method for GSH determination from cell organelles. Results: The GSH level of organelles could easily be measured by the monochlorobimane-HPLC-fluorescent method. The addition of monochlorobimane to the homogenisation buffer prevented the oxidation of GSH during isolation. The formation of monochlorobimane-GSH adduct was accelerated by the intrinsic GST activity of samples, however the omission of GST from the GSH standards could cause the overestimation of GSH content of biological samples. NEM is an excellent thiol protective agent and the GSH-NEM conjugate can be directly analysed by HPLC-UV, but the relatively high limit of detection made the method unsuitable for the determination of GSH from cell organelles. Although the DTNB-GSH recycling assay is quite simple and rapid the stabilization of GSH and the efficiency of detection lag behind the monochlorobimane-HPLC-fluorescent method. Discussion: The monochlorobimane-HPLC-fluorescent method can be advised for the determination of GSH from pharmacologically and toxicological relevant cell organelles and liver tissue whilst addition of monochlorobimane to the homogenisation buffer prevented the autoxidation of GSH.
Language	English
Publishing date	2017-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1105919-9
ISSN	1873-488X ; 1056-8719
ISSN (online)	1873-488X
ISSN	1056-8719
DOI	10.1016/j.vascn.2017.05.004
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Article: The determination of hepatic glutathione at tissue and subcellular level

Lőrincz, Tamás / Szarka, András

Journal of pharmacological and toxicological methods. 2017 Nov., v. 88

2017

Abstract: Glutathione (GSH) through its important function in the antioxidant protection of cells and in the conjugation of drugs and xenobiotics has crucial importance in pharmacology and toxicology. Since GSH is most often measured in liver tissue and different ... ...

Abstract	Glutathione (GSH) through its important function in the antioxidant protection of cells and in the conjugation of drugs and xenobiotics has crucial importance in pharmacology and toxicology. Since GSH is most often measured in liver tissue and different cell organelles it is important to choose the method that best suits for the determination of GSH.The GSH content of cell organelles isolated from control and BSO-treated liver tissues was determined by the GSH-NEM-HPLC-UV, monochlorobimane-GSH-HPLC-fluorescence method and DTNB-GSH recycling assay to find the most suitable method for GSH determination from cell organelles.The GSH level of organelles could easily be measured by the monochlorobimane-HPLC-fluorescent method. The addition of monochlorobimane to the homogenisation buffer prevented the oxidation of GSH during isolation. The formation of monochlorobimane-GSH adduct was accelerated by the intrinsic GST activity of samples, however the omission of GST from the GSH standards could cause the overestimation of GSH content of biological samples. NEM is an excellent thiol protective agent and the GSH-NEM conjugate can be directly analysed by HPLC-UV, but the relatively high limit of detection made the method unsuitable for the determination of GSH from cell organelles. Although the DTNB-GSH recycling assay is quite simple and rapid the stabilization of GSH and the efficiency of detection lag behind the monochlorobimane-HPLC-fluorescent method.The monochlorobimane-HPLC-fluorescent method can be advised for the determination of GSH from pharmacologically and toxicological relevant cell organelles and liver tissue whilst addition of monochlorobimane to the homogenisation buffer prevented the autoxidation of GSH.
Keywords	antioxidants ; autoxidation ; detection limit ; glutathione ; homogenization ; liver ; organelles ; thiols ; toxicology ; xenobiotics
Language	English
Dates of publication	2017-11
Size	p. 32-39.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1105919-9
ISSN	1873-488X ; 1056-8719
ISSN (online)	1873-488X
ISSN	1056-8719
DOI	10.1016/j.vascn.2017.05.004
Database	NAL-Catalogue (AGRICOLA)

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