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Article ; Online: The vitamin B

Tat, John / Chang, Stephen C / Link, Cole D / Razo-Lopez, Suelen / Ingerto, Michael J / Katebian, Behdod / Chan, Adriano / Kalyanaraman, Hema / Pilz, Renate B / Boss, Gerry R

Clinical toxicology (Philadelphia, Pa.)

2023 Volume 61, Issue 4, Page(s) 212–222

Abstract: Context: The azide anion (N: Results: We found cobinamide bound azide with a moderate affinity (K: Conclusion: We conclude cobinamide likely acted by neutralizing both oxidative stress and nitric oxide, and that it should be given further ... ...

Abstract	Context: The azide anion (N Results: We found cobinamide bound azide with a moderate affinity (K Conclusion: We conclude cobinamide likely acted by neutralizing both oxidative stress and nitric oxide, and that it should be given further consideration as an azide antidote.
MeSH term(s)	Mice ; Animals ; Vitamin B 12 ; Drosophila melanogaster/metabolism ; Azides/metabolism ; Antidotes/pharmacology ; Nitric Oxide ; Electron Transport Complex IV/metabolism ; Cobamides ; Hypotension ; Adenosine Triphosphate ; Vitamins ; Mammals/metabolism
Chemical Substances	Vitamin B 12 (P6YC3EG204) ; cobinamide (13497-85-3) ; Azides ; Antidotes ; Nitric Oxide (31C4KY9ESH) ; Electron Transport Complex IV (EC 1.9.3.1) ; Cobamides ; Adenosine Triphosphate (8L70Q75FXE) ; Vitamins
Language	English
Publishing date	2023-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	204476-6
ISSN	1556-9519 ; 0009-9309 ; 0731-3810 ; 1556-3650
ISSN (online)	1556-9519
ISSN	0009-9309 ; 0731-3810 ; 1556-3650
DOI	10.1080/15563650.2023.2185125
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Article ; Online: Aortic pathology from protein kinase G activation is prevented by an antioxidant vitamin B

Schwaerzer, Gerburg K / Kalyanaraman, Hema / Casteel, Darren E / Dalton, Nancy D / Gu, Yusu / Lee, Seunghoe / Zhuang, Shunhui / Wahwah, Nisreen / Schilling, Jan M / Patel, Hemal H / Zhang, Qian / Makino, Ayako / Milewicz, Dianna M / Peterson, Kirk L / Boss, Gerry R / Pilz, Renate B

Nature communications

2019 Volume 10, Issue 1, Page(s) 3533

Abstract: People heterozygous for an activating mutation in protein kinase G1 (PRKG1, p.Arg177Gln) develop thoracic aortic aneurysms and dissections (TAAD) as young adults. Here we report that mice heterozygous for the mutation have a three-fold increase in basal ... ...

Abstract	People heterozygous for an activating mutation in protein kinase G1 (PRKG1, p.Arg177Gln) develop thoracic aortic aneurysms and dissections (TAAD) as young adults. Here we report that mice heterozygous for the mutation have a three-fold increase in basal protein kinase G (PKG) activity, and develop age-dependent aortic dilation. Prkg1
MeSH term(s)	Acetylcysteine/administration & dosage ; Aneurysm, Dissecting/genetics ; Aneurysm, Dissecting/pathology ; Aneurysm, Dissecting/prevention & control ; Animals ; Aorta, Thoracic/diagnostic imaging ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/pathology ; Aortic Aneurysm, Thoracic/genetics ; Aortic Aneurysm, Thoracic/pathology ; Aortic Aneurysm, Thoracic/prevention & control ; Cobamides/administration & dosage ; Cyclic GMP-Dependent Protein Kinase Type I/genetics ; Cyclic GMP-Dependent Protein Kinase Type I/metabolism ; Disease Models, Animal ; Echocardiography ; Female ; Free Radical Scavengers/administration & dosage ; Gain of Function Mutation ; Gene Knock-In Techniques ; HEK293 Cells ; Humans ; Male ; Marfan Syndrome/complications ; Marfan Syndrome/genetics ; Mice ; Mice, Transgenic ; Myocytes, Smooth Muscle ; Oxidative Stress/drug effects ; Oxidative Stress/genetics ; Primary Cell Culture
Chemical Substances	Cobamides ; Free Radical Scavengers ; cobinamide (13497-85-3) ; Cyclic GMP-Dependent Protein Kinase Type I (EC 2.7.11.12) ; PRKG1 protein, human (EC 2.7.11.12) ; Prkg1 protein, mouse (EC 2.7.11.12) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2019-08-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-11389-1
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Article ; Online: A physiological dose of oral vitamin B-12 improves hematological, biochemical-metabolic indices and peripheral nerve function in B-12 deficient Indian adolescent women.

Yajnik, Chittaranjan S / Behere, Rishikesh V / Bhat, Dattatray S / Memane, Nilam / Raut, Deepa / Ladkat, Rasika / Yajnik, Pallavi C / Kumaran, Kalyanaraman / Fall, Caroline H D

PloS one

2019 Volume 14, Issue 10, Page(s) e0223000

Abstract: Background: Vitamin B-12 deficiency is often considered synonymous with pernicious anemia, a rare ... In developing countries such as India, inadequate dietary intake of B-12 due to socio-cultural factors leads to widely ... prevalent asymptomatic low B-12 status. In this scenario, lower doses of oral B-12 may be effective, safer ...

Abstract	Background: Vitamin B-12 deficiency is often considered synonymous with pernicious anemia, a rare condition in which severe malabsorption of the vitamin requires high-dose parenteral treatment. In developing countries such as India, inadequate dietary intake of B-12 due to socio-cultural factors leads to widely prevalent asymptomatic low B-12 status. In this scenario, lower doses of oral B-12 may be effective, safer and more affordable. Objective: To examine the effects of oral B-12 treatment at physiological doses on hematological and biochemical indices and peripheral nerve function in B-12 deficient rural Indian adolescent women. Methods: Thirty-nine women with B-12 deficiency who were excluded from a community based B-12 supplementation trial (Pune Rural Intervention in Young Adolescents (PRIYA)) received oral B-12 2μg/day, either alone (n = 19) or with multiple micronutrients (UNIMAPP formula + 20gm milk powder, n = 20) for 11 months. Hematological indices, nutrients (B-12, folate), metabolites (homocysteine) and peripheral nerve function (SUDOSCAN, Impetomedical, Paris and sensory nerve conduction velocity (NCV) of median and sural nerves) were assessed at baseline and after 11 months of B-12 treatment. Results: Results were similar in the two treatment allocation groups, which were therefore combined. At baseline, all women had B-12 concentration <100pmol/L, 79% were anemic and 33% had macrocytosis, but none had neuropathy. After 11 months of treatment, B-12 levels increased, while folate did not change. The prevalence of anemia fell to 59% and mean corpuscular volume (MCV) and plasma homocysteine concentrations decreased. Sudomotor nerve function in the feet improved by an average of 14.7%, and sensory conduction velocity in median and sural nerves increased by 16.2% and 29.4% respectively. Conclusion: We document clinically beneficial effects of supplementation with a physiological dose of oral B-12 in asymptomatic rural Indian adolescent women with very low B-12 status. These findings support a public health approach to tackle the widely prevalent low B-12 status in young Indians.
MeSH term(s)	Administration, Oral ; Adolescent ; Dietary Supplements ; Female ; Folic Acid/blood ; Humans ; India/epidemiology ; Micronutrients/blood ; Micronutrients/deficiency ; Nutritional Status ; Peripheral Nerves/drug effects ; Peripheral Nerves/physiology ; Rural Population ; Vitamin B 12/administration & dosage ; Vitamin B 12/blood ; Vitamin B 12 Deficiency/blood ; Vitamin B 12 Deficiency/drug therapy ; Vitamin B 12 Deficiency/epidemiology ; Vitamin B 12 Deficiency/pathology ; Vitamin B Complex/administration & dosage
Chemical Substances	Micronutrients ; Vitamin B Complex (12001-76-2) ; Folic Acid (935E97BOY8) ; Vitamin B 12 (P6YC3EG204)
Language	English
Publishing date	2019-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0223000
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Article ; Online: NAC, NAC, Knockin' on Heaven's door: Interpreting the mechanism of action of N-acetylcysteine in tumor and immune cells.

Kalyanaraman, Balaraman

Redox biology

2022 Volume 57, Page(s) 102497

Abstract: N-acetylcysteine (NAC) has been used as a direct scavenger of reactive oxygen species (hydrogen peroxide, in particular) and an antioxidant in cancer biology and immuno-oncology. NAC is the antioxidant drug most frequently employed in studies using tumor ...

Abstract	N-acetylcysteine (NAC) has been used as a direct scavenger of reactive oxygen species (hydrogen peroxide, in particular) and an antioxidant in cancer biology and immuno-oncology. NAC is the antioxidant drug most frequently employed in studies using tumor cells, immune cells, and preclinical mouse xenografts. Most studies use redox-active fluorescent probes such as dichlorodihydrofluorescein, hydroethidine, mitochondria-targeted hydroethidine, and proprietary kit-based probes (i.e., CellROX Green and CellROX Red) for intracellular detection of superoxide or hydrogen peroxide. Inhibition of fluorescence by NAC was used as a key experimental observation to support the formation of reactive oxygen species and redox mechanisms proposed for ferroptosis, tumor metastasis, and redox signaling in the tumor microenvironment. Reactive oxygen species such as superoxide and hydrogen peroxide stimulate or abrogate tumor cells and immune cells depending on multiple factors. Understanding the mechanism of antioxidants is crucial for interpretation of the results. Because neither NAC nor the fluorescent probes indicated above react directly with hydrogen peroxide, it is critically important to reinterpret the results to advance our understanding of the mechanism of action of NAC and shed additional mechanistic insight on redox-regulated signaling in tumor biology. To this end, this review is focused on how NAC could affect multiple pathways in cancer cells, including iron signaling, ferroptosis, and the glutathione-dependent antioxidant and redox signaling mechanism, and how NAC could inhibit oxidation of the fluorescent probes through multiple mechanisms.
Language	English
Publishing date	2022-10-09
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102497
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Article ; Online: Exploiting the tumor immune microenvironment and immunometabolism using mitochondria-targeted drugs: Challenges and opportunities in racial disparity and cancer outcome research.

Kalyanaraman, Balaraman

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2022 Volume 36, Issue 4, Page(s) e22226

Abstract: Black and Hispanic cancer patients have a higher incidence of cancer mortality. Many factors (e.g., socioeconomic differences, insufficient access to healthcare) contribute to racial disparity. Emerging research implicates biological disparity in cancer ... ...

Abstract	Black and Hispanic cancer patients have a higher incidence of cancer mortality. Many factors (e.g., socioeconomic differences, insufficient access to healthcare) contribute to racial disparity. Emerging research implicates biological disparity in cancer outcomes. Studies show distinct differences in the tumor immune microenvironment (TIME) in Black cancer patients. Studies also have linked altered mitochondrial metabolism to changes in immune cell activation in TIME. Recent publications revealed a novel immunomodulatory role for triphenylphosphonium-based mitochondrial-targeted drugs (MTDs). These are synthetically modified, naturally occurring molecules (e.g., honokiol, magnolol, metformin) or FDA-approved small molecule drugs (e.g., atovaquone, hydroxyurea). Modifications involve conjugating the parent molecule via an alkyl linker chain to a triphenylphosphonium moiety. These modified molecules (e.g., Mito-honokiol, Mito-magnolol, Mito-metformin, Mito-atovaquone, Mito-hydroxyurea) accumulate in tumor cell mitochondria more effectively than in normal cells and inhibit mitochondrial respiration, induce reactive oxygen species, activate AMPK and redox transcription factors, and inhibit cancer cell proliferation. Besides these intrinsic effects of MTDs in redox signaling and proliferation in tumors, MTDs induced extrinsic effects in the TIME of mouse xenografts. MTD treatment inhibited tumor-suppressive immune cells, myeloid-derived suppressor cells, and regulatory T cells, and activated T cells and antitumor immune effects. One key biological disparity in Black cancer patients was related to altered mitochondrial oxidative metabolism; MTDs targeting vulnerabilities in tumor cells and the TIME may help us understand this biological disparity. Clinical trials should include an appropriate number of Black and Hispanic cancer patients and should validate the intratumoral, antihypoxic effects of MTDs with imaging.
MeSH term(s)	Atovaquone/pharmacology ; Atovaquone/therapeutic use ; Biphenyl Compounds/pharmacology ; Biphenyl Compounds/therapeutic use ; Blacks ; Health Status Disparities ; Hispanic or Latino ; Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Lignans/pharmacology ; Lignans/therapeutic use ; Mitochondria/drug effects ; Neoplasms/drug therapy ; Neoplasms/ethnology ; Neoplasms/immunology ; Neoplasms/metabolism ; Oxidative Phosphorylation/drug effects ; Tumor Microenvironment
Chemical Substances	Biphenyl Compounds ; Immune Checkpoint Inhibitors ; Lignans ; magnolol (001E35HGVF) ; honokiol (11513CCO0N) ; Atovaquone (Y883P1Z2LT)
Language	English
Publishing date	2022-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202101862R
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Reactive oxygen species, proinflammatory and immunosuppressive mediators induced in COVID-19: overlapping biology with cancer.

Kalyanaraman, Balaraman

RSC chemical biology

2021 Volume 2, Issue 5, Page(s) 1402–1414

Abstract: This review analyzes the published literature linking the different mechanisms focused on oxidative stress and inflammation that contribute to COVID-19 disease severity. The objective is to bring together potential proinflammatory mechanisms of COVID-19 ... ...

Abstract	This review analyzes the published literature linking the different mechanisms focused on oxidative stress and inflammation that contribute to COVID-19 disease severity. The objective is to bring together potential proinflammatory mechanisms of COVID-19 pathogenesis and address mitigation strategies using naturally occurring compounds and FDA-approved drugs. Outstanding questions addressed include the following: What is the mechanistic basis for linking enhanced vulnerability in COVID-19 to increased oxidative damage and proinflammatory mediators (
Language	English
Publishing date	2021-06-30
Publishing country	England
Document type	Journal Article ; Review
ISSN	2633-0679
ISSN (online)	2633-0679
DOI	10.1039/d1cb00042j
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Article ; Online: A physiological dose of oral vitamin B-12 improves hematological, biochemical-metabolic indices and peripheral nerve function in B-12 deficient Indian adolescent women.

Chittaranjan S Yajnik / Rishikesh V Behere / Dattatray S Bhat / Nilam Memane / Deepa Raut / Rasika Ladkat / Pallavi C Yajnik / Kalyanaraman Kumaran / Caroline H D Fall

PLoS ONE, Vol 14, Iss 10, p e

2019 Volume 0223000

Abstract: Background Vitamin B-12 deficiency is often considered synonymous with pernicious anemia, a rare ... In developing countries such as India, inadequate dietary intake of B-12 due to socio-cultural factors leads to widely ... prevalent asymptomatic low B-12 status. In this scenario, lower doses of oral B-12 may be effective, safer ...

Abstract	Background Vitamin B-12 deficiency is often considered synonymous with pernicious anemia, a rare condition in which severe malabsorption of the vitamin requires high-dose parenteral treatment. In developing countries such as India, inadequate dietary intake of B-12 due to socio-cultural factors leads to widely prevalent asymptomatic low B-12 status. In this scenario, lower doses of oral B-12 may be effective, safer and more affordable. Objective To examine the effects of oral B-12 treatment at physiological doses on hematological and biochemical indices and peripheral nerve function in B-12 deficient rural Indian adolescent women. Methods Thirty-nine women with B-12 deficiency who were excluded from a community based B-12 supplementation trial (Pune Rural Intervention in Young Adolescents (PRIYA)) received oral B-12 2μg/day, either alone (n = 19) or with multiple micronutrients (UNIMAPP formula + 20gm milk powder, n = 20) for 11 months. Hematological indices, nutrients (B-12, folate), metabolites (homocysteine) and peripheral nerve function (SUDOSCAN, Impetomedical, Paris and sensory nerve conduction velocity (NCV) of median and sural nerves) were assessed at baseline and after 11 months of B-12 treatment. Results Results were similar in the two treatment allocation groups, which were therefore combined. At baseline, all women had B-12 concentration <100pmol/L, 79% were anemic and 33% had macrocytosis, but none had neuropathy. After 11 months of treatment, B-12 levels increased, while folate did not change. The prevalence of anemia fell to 59% and mean corpuscular volume (MCV) and plasma homocysteine concentrations decreased. Sudomotor nerve function in the feet improved by an average of 14.7%, and sensory conduction velocity in median and sural nerves increased by 16.2% and 29.4% respectively. Conclusion We document clinically beneficial effects of supplementation with a physiological dose of oral B-12 in asymptomatic rural Indian adolescent women with very low B-12 status. These findings support a public ...
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Teaching the basics of repurposing mitochondria-targeted drugs: From Parkinson's disease to cancer and back to Parkinson's disease.

Kalyanaraman, Balaraman

Redox biology

2020 Volume 36, Page(s) 101665

Abstract: Parkinson's disease (PD) and cancer share common mutations in mitochondrial proteins: Parkin and PINK1. The overlapping of genes involved in PD and cancer implies that the two diseases might share a common pathogenic mechanism. There are other compelling ...

Abstract	Parkinson's disease (PD) and cancer share common mutations in mitochondrial proteins: Parkin and PINK1. The overlapping of genes involved in PD and cancer implies that the two diseases might share a common pathogenic mechanism. There are other compelling rationales for a mechanistic link between these diseases. Mitochondria and autophagy/mitophagy are emerging as therapeutic targets in PD and cancer: Ongoing research in our laboratories has shown that, when administered early, mitochondria-targeted agents afford neuroprotection in preclinical mice models of PD. Also, we discovered that mitochondria-targeted drugs inhibit tumor cell proliferation. We propose that mitochondrial targeting stimulates conservation of cellular energy critical for neuronal cell survival, whereas the energy conservation mechanism inhibits proliferation of cancer cells by depriving the energy necessary for cancer cell growth. We propose a promising drug repurposing strategy involving mitochondria-targeted drugs synthesized from naturally occurring molecules and FDA-approved drugs that are relatively nontoxic in both PD and cancer. These compounds have been shown to induce various cellular signaling pathways for autophagy/mitophagy, anti-inflammatory, and immunomodulatory effects that are implicated as therapeutic mechanisms in PD and cancer.
MeSH term(s)	Animals ; Drug Repositioning ; Mice ; Mitochondria ; Neoplasms/drug therapy ; Neoplasms/genetics ; Parkinson Disease/drug therapy ; Pharmaceutical Preparations ; Protein Kinases
Chemical Substances	Pharmaceutical Preparations ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2020-08-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101665
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Article ; Online: Do free radical NETwork and oxidative stress disparities in African Americans enhance their vulnerability to SARS-CoV-2 infection and COVID-19 severity?

Kalyanaraman, Balaraman

Redox biology

2020 Volume 37, Page(s) 101721

Abstract: This review focuses on the hypothetical mechanisms for enhanced vulnerability of African Americans to SARS-CoV-2 infection, COVID-19 severity, and increased deaths. A disproportionately higher number of African Americans are afflicted with autoimmune and ...

Abstract	This review focuses on the hypothetical mechanisms for enhanced vulnerability of African Americans to SARS-CoV-2 infection, COVID-19 severity, and increased deaths. A disproportionately higher number of African Americans are afflicted with autoimmune and inflammatory diseases (e.g., diabetes, hypertension, obesity), and SARS-CoV-2 has helped expose these health disparities. Several factors including socioeconomic status, inferior health care, and work circumstances contribute to these disparities. Identifying potential inflammatory biomarkers and decreasing basal levels in high-risk individuals with comorbidities through preventive measures is critical. Immune cells, particularly neutrophils, protect us against pathogens (bacteria, fungi, and viruses) through increased generation of free radicals or oxidants and neutrophil extracellular traps (NETs) that ensnare pathogens, killing them extracellularly. However, continued generation of NETs coupled with the lack of prompt removal pose danger to host cells. NET levels are increased during pro-inflammatory diseases. COVID-19 patients exhibit elevated NET levels, depending upon disease severity. Conceivably, high-risk individuals with elevated basal NET levels would exhibit hyper-inflammation when infected with SARS-CoV-2, amplifying disease severity and deaths. Drugs inhibiting oxidant formation and vitamin supplements decreased NET formation in mice models of inflammation. Thus, it is conceivable that preventive treatments lowering NET levels and inflammation in high-risk individuals could mitigate SARS-CoV-2-induced complications and decrease mortality.
MeSH term(s)	Black or African American ; Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; COVID-19/epidemiology ; COVID-19/metabolism ; Drug Repositioning ; Extracellular Traps/drug effects ; Extracellular Traps/metabolism ; Free Radicals/metabolism ; Humans ; Inflammation/drug therapy ; Inflammation/epidemiology ; Inflammation/metabolism ; Neutrophils/drug effects ; Neutrophils/metabolism ; Oxidative Stress/drug effects ; Risk Factors ; SARS-CoV-2/drug effects ; SARS-CoV-2/physiology ; COVID-19 Drug Treatment
Chemical Substances	Antioxidants ; Free Radicals
Keywords	covid19
Language	English
Publishing date	2020-09-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101721
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Article ; Online: Teaching the basics of the mechanism of doxorubicin-induced cardiotoxicity: Have we been barking up the wrong tree?

Kalyanaraman, Balaraman

Redox biology

2019 Volume 29, Page(s) 101394

Abstract: Doxorubicin (DOX), or Adriamycin, an anthracycline antibiotic discovered serendipitously as a chemotherapeutic drug several decades ago, is still one of the most effective drugs for treating various adult and pediatric cancers (breast cancer, Hodgkin's ... ...

Abstract	Doxorubicin (DOX), or Adriamycin, an anthracycline antibiotic discovered serendipitously as a chemotherapeutic drug several decades ago, is still one of the most effective drugs for treating various adult and pediatric cancers (breast cancer, Hodgkin's disease, lymphoblastic leukemia). However, one of the major side effects of the continuous use of DOX is dose-dependent, long-term, and potentially lethal cardiovascular toxicity (congestive heart failure and cardiomyopathy) in cancer survivors many years after cessation of chemotherapy. In addition, predisposition to cardiotoxicity varied considerably among individuals. The long-held notion that DOX cardiotoxicity is caused by reactive oxygen species formed from the redox-cycling of DOX semiquinone lacks rigorous proof in a chronic animal model, and administration of reactive oxygen species detoxifying agents failed to reverse DOX-induced cardiac problems. In this review, I discuss the pros and cons of the reactive oxygen species pathway as a primary or secondary mechanism of DOX cardiotoxicity, the role of topoisomerases, and the potential use of mitochondrial-biogenesis-enhancing compounds in reversing DOX-induced cardiomyopathy. New approaches for well-designed clinical trials that repurpose FDA-approved drugs and naturally occurring polyphenolic compounds prophylactically to prevent or mitigate cardiovascular complications in both pediatric and adult cancer survivors are needed. Essentially, the focus should be on enhancing mitochondrial biogenesis to prevent or mitigate DOX-induced cardiotoxicity.
MeSH term(s)	Animals ; Antibiotics, Antineoplastic/toxicity ; Cardiotoxicity ; Child ; Doxorubicin/toxicity ; Humans ; Reactive Oxygen Species ; Topoisomerase II Inhibitors
Chemical Substances	Antibiotics, Antineoplastic ; Reactive Oxygen Species ; Topoisomerase II Inhibitors ; Doxorubicin (80168379AG)
Language	English
Publishing date	2019-11-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2019.101394
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