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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

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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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: 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 repurposing mitochondria-targeted drugs

Balaraman Kalyanaraman

Redox Biology, Vol 36, Iss , Pp 101665- (2020)

From Parkinson's disease to cancer and back to Parkinson's disease

2020

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.
Keywords	Mitochondria-targeting drugs ; Mitophagy ; Autophagy ; Parkinson's disease ; Neuroprotection ; Antitumor effects ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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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?

Balaraman Kalyanaraman

Redox Biology, Vol 37, Iss , Pp 101721- (2020)

2020

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.
Keywords	Coronavirus ; COVID-19 ; Oxidants ; Neutrophils ; African Americans ; Black Americans ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Teaching the basics of the mechanism of doxorubicin-induced cardiotoxicity

Balaraman Kalyanaraman

Redox Biology, Vol 29, Iss , Pp - (2020)

Have we been barking up the wrong tree?

2020

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. Keywords: Chemotherapy, Reactive oxygen species, Topoisomerase, Mitochondrial biogenesis, Cardio-oncology, Cardioprotection
Keywords	Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Gut microbiome, short-chain fatty acids, alpha-synuclein, neuroinflammation, and ROS/RNS: Relevance to Parkinson's disease and therapeutic implications.

Kalyanaraman, Balaraman / Cheng, Gang / Hardy, Micael

Redox biology

2024 Volume 71, Page(s) 103092

Abstract: In this review, we explore how short-chain fatty acids (SCFAs) produced by the gut microbiome affect Parkinson's disease (PD) through their modulatory interactions with alpha-synuclein, neuroinflammation, and oxidative stress mediated by reactive oxygen ... ...

Abstract	In this review, we explore how short-chain fatty acids (SCFAs) produced by the gut microbiome affect Parkinson's disease (PD) through their modulatory interactions with alpha-synuclein, neuroinflammation, and oxidative stress mediated by reactive oxygen and nitrogen species (ROS/RNS). In particular, SCFAs-such as acetate, propionate, and butyrate-are involved in gut-brain communication and can modulate alpha-synuclein aggregation, a hallmark of PD. The gut microbiome of patients with PD has lower levels of SCFAs than healthy individuals. Probiotics may be a potential strategy to restore SCFAs and alleviate PD symptoms, but the underlying mechanisms are not fully understood. Also in this review, we discuss how alpha-synuclein, present in the guts and brains of patients with PD, may induce neuroinflammation and oxidative stress via ROS/RNS. Alpha-synuclein is considered an early biomarker for PD and may link the gut-brain axis to the disease pathogenesis. Therefore, elucidating the role of SCFAs in the gut microbiome and their impact on alpha-synuclein-induced neuroinflammation in microglia and on ROS/RNS is crucial in PD pathogenesis and treatment.
MeSH term(s)	Humans ; alpha-Synuclein ; Fatty Acids, Volatile ; Gastrointestinal Microbiome ; Neuroinflammatory Diseases ; Oxygen ; Parkinson Disease/etiology ; Parkinson Disease/therapy ; Parkinson Disease/pathology ; Reactive Nitrogen Species ; Reactive Oxygen Species
Chemical Substances	alpha-Synuclein ; Fatty Acids, Volatile ; Oxygen (S88TT14065) ; Reactive Nitrogen Species ; Reactive Oxygen Species ; SNCA protein, human
Language	English
Publishing date	2024-02-16
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.2024.103092
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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 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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