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Lapachone AND nad+ ratio

Moon Hee Jeong, Jin Hwan Kim, Kang-Sik Seo, Tae Hwan Kwak, Woo Jin Park
Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is a mitochondrial disease caused by mutations in the mitochondrial genome. This study investigated the efficacy of β-lapachone (β-lap), a natural quinone compound, in rescuing mitochondrial dysfunction in MELAS cybrid cells. β-Lap significantly restored energy production and mitochondrial membrane potential as well as normalized the elevated ROS level in MELAS cybrid cells. Additionally, β-lap reduced lactic acidosis and restored glucose uptake in the MELAS cybrid cells...
November 21, 2014: Biochemical and Biophysical Research Communications
Yong-Hoon Kim, Jung Hwan Hwang, Kyoung-Shim Kim, Jung-Ran Noh, Gil-Tae Gang, Youngwon Seo, Ki-Hoan Nam, Tae Hwan Kwak, Hee Gu Lee, Chul-Ho Lee
BACKGROUND: Endothelial nitric oxide synthase (eNOS) is involved in blood pressure (BP) regulation through the production of nitric oxide. Sirtuin I (SIRT1), an NAD-dependent protein deacetylase, promotes vascular relaxation through deacetylation and activation of eNOS. β-Lapachone (βL) increases the cellular NAD(+)/NADH ratio by activating NAD(P)H: quinone oxidoreductase 1 (NQO1). In this study, we verified whether activation of NQO1 by βL modulates BP through regulation of eNOS acetylation in a hypertensive animal model...
January 2015: American Journal of Hypertension
Lifen Cao, Long Shan Li, Christopher Spruell, Ling Xiao, Gaurab Chakrabarti, Erik A Bey, Kathryn E Reinicke, Melissa C Srougi, Zachary Moore, Ying Dong, Peggy Vo, Wareef Kabbani, Chin-Rang Yang, Xiaoyu Wang, Farjana Fattah, Julio C Morales, Edward A Motea, William G Bornmann, John S Yordy, David A Boothman
AIMS: β-Lapachone (β-lap), a novel radiosensitizer with potent antitumor efficacy alone, selectively kills solid cancers that over-express NAD(P)H: quinone oxidoreductase 1 (NQO1). Since breast or other solid cancers have heterogeneous NQO1 expression, therapies that reduce the resistance (e.g., NQO1(low)) of tumor cells will have significant clinical advantages. We tested whether NQO1-proficient (NQO1(+)) cells generated sufficient hydrogen peroxide (H2O2) after β-lap treatment to elicit bystander effects, DNA damage, and cell death in neighboring NQO1(low) cells...
July 10, 2014: Antioxidants & Redox Signaling
Sanghee Shin, Jisoo Park, Yuwen Li, Ki Nam Min, Gyeyeong Kong, Gang Min Hur, Jin Man Kim, Minho Shong, Min-Suk Jung, Jong Kook Park, Kyeong-Hoon Jeong, Myoung Gyu Park, Tae Hwan Kwak, Derek P Brazil, Jongsun Park
UNLABELLED: Alcohol-induced liver injury is the most common liver disease in which fatty acid metabolism is altered. It is thought that altered NAD(+)/NADH redox potential by alcohol in the liver causes fatty liver by inhibiting fatty acid oxidation and the activity of tricarboxylic acid cycle reactions. β-Lapachone (βL), a naturally occurring quinone, has been shown to stimulate fatty acid oxidation in an obese mouse model by activating adenosine monophosphate-activated protein kinase (AMPK)...
February 2014: Cellular Signalling
Yong-Hoon Kim, Jung Hwan Hwang, Kyung-Shim Kim, Jung-Ran Noh, Gil-Tae Gang, Won Keun Oh, Kyeong-Hoon Jeong, Tae Hwan Kwak, Hueng-Sik Choi, In-Kyu Lee, Chul-Ho Lee
AIMS: Guanosine 5'-triphosphate cyclohydrolase-1 (GTPCH-1) is a rate-limiting enzyme in de-novo synthesis of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS) coupling. Adenosine 5'-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation...
February 2014: Journal of Hypertension
Gil-Tae Gang, Jung Hwan Hwang, Yong-Hoon Kim, Jung-Ran Noh, Kyoung-Shim Kim, Jin Young Jeong, Dae Eun Choi, Kang Wook Lee, Ju-Young Jung, Minho Shong, Chul-Ho Lee
UNLABELLED: Ischemia/reperfusion (I/R) is the most common cause of acute renal injury. I/R-induced reactive oxygen species (ROS) are thought to be a major factor in the development of acute renal injury by promoting the initial tubular damage. NAD(P)H: quinone oxidoreductase 1 (NQO1) is a well-known antioxidant protein that regulates ROS generation. The purpose of this study was to investigate whether NQO1 modulates the renal I/R injury (IRI) associated with NADPH oxidase (NOX)-derived ROS production in an animal model...
February 2014: Free Radical Biology & Medicine
Gi-Su Oh, Hyung-Jin Kim, Jae-Hyuck Choi, Aihua Shen, Seong-Kyu Choe, Anzani Karna, Seung Hoon Lee, Hyang-Jeong Jo, Sei-Hoon Yang, Tae Hwan Kwak, Chul-Ho Lee, Raekil Park, Hong-Seob So
UNLABELLED: Cisplatin is a widely used chemotherapeutic agent for the treatment of various tumors. In addition to its antitumor activity, cisplatin affects normal cells and may induce adverse effects, such as ototoxicity, nephrotoxicity, and neuropathy. Various mechanisms, such as DNA adduct formation, mitochondrial dysfunction, oxidative stress, and inflammatory responses, are critically involved in cisplatin-induced adverse effects. As NAD(+) is a cofactor for various enzymes associated with cellular homeostasis, we studied the effects of increased NAD(+) levels by means of NAD(P)H: quinone oxidoreductase 1 (NQO1) activation using a known pharmacological activator (β-lapachone) in wild-type and NQO1(-/-) mice on cisplatin-induced renal dysfunction in vivo...
March 2014: Kidney International
Erik A Bey, Kathryn E Reinicke, Melissa C Srougi, Marie Varnes, Vernon E Anderson, John J Pink, Long Shan Li, Malina Patel, Lifen Cao, Zachary Moore, Amy Rommel, Michael Boatman, Cheryl Lewis, David M Euhus, William G Bornmann, Donald J Buchsbaum, Douglas R Spitz, Jinming Gao, David A Boothman
Improving patient outcome by personalized therapy involves a thorough understanding of an agent's mechanism of action. β-Lapachone (clinical forms, Arq501/Arq761) has been developed to exploit dramatic cancer-specific elevations in the phase II detoxifying enzyme NAD(P)H:quinone oxidoreductase (NQO1). NQO1 is dramatically elevated in solid cancers, including primary and metastatic [e.g., triple-negative (ER-, PR-, Her2/Neu-)] breast cancers. To define cellular factors that influence the efficacy of β-lapachone using knowledge of its mechanism of action, we confirmed that NQO1 was required for lethality and mediated a futile redox cycle where ∼120 moles of superoxide were formed per mole of β-lapachone in 2 minutes...
October 2013: Molecular Cancer Therapeutics
Yong-Hoon Kim, Jung Hwan Hwang, Kyung-Shim Kim, Jung-Ran Noh, Gil-Tae Gang, Sang-Woo Kim, Seung Pil Jang, Sang-Ju Lee, Sung-Ho Her, Kyeong-Hoon Jeong, Tae Hwan Kwak, Woo Jin Park, Irina V Balyasnikova, Minho Shong, Chul-Ho Lee
AIMS: Angiotensin-converting enzyme (ACE) plays a key role in blood pressure (BP) homeostasis via regulation of angiotensin II. Active ACE ectodomain is enzymatically cleaved and released into body fluids, including plasma, and elevated plasma ACE levels are associated with increased BP. β-lapachone (βL) has been shown to increase cellular NAD(+)/NADH ratio via activation of NAD(P)H:quinone oxidoreductase 1 (NQO1). In this study, we evaluated whether NQO1 activation by βL modulates BP through regulation of ACE shedding in an animal model of hypertension...
September 1, 2013: Cardiovascular Research
Jeong-sook Lee, Ah Hyung Park, Sang-Hee Lee, Seoung-Hoon Lee, Jin-Hwan Kim, Suk-Jin Yang, Young Il Yeom, Tae Hwan Kwak, Dongyeop Lee, Seung-Jae Lee, Chul-Ho Lee, Jin Man Kim, Daesoo Kim
NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR). Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented age-dependent decline of motor and cognitive function in aged mice. βL-fed mice did not alter their food-intake or locomotor activity but did increase their energy expenditure as measured by oxygen consumption and heat generation...
2012: PloS One
Yong-Hoon Kim, Jung Hwan Hwang, Jung-Ran Noh, Gil-Tae Gang, Surendar Tadi, Yong-Hyeon Yim, Nam Ho Jeoung, Tae Hwan Kwak, Sang-Hee Lee, Gi Ryang Kweon, Jin-Man Kim, Minho Shong, In-Kyu Lee, Chul-Ho Lee
NADPH oxidase (NOX) is a predominant source of reactive oxygen species (ROS), and the activity of NOX, which uses NADPH as a common rate-limiting substrate, is upregulated by prolonged dietary salt intake. β-Lapachone (βL), a well-known substrate of NAD(P)H:quinone oxidoreductase 1 (NQO1), decreases the cellular NAD(P)H/NAD(P)(+) ratio via activation of NQO1. In this study, we evaluated whether NQO1 activation by βL modulates salt-induced renal injury associated with NOX-derived ROS regulation in an animal model...
March 1, 2012: Free Radical Biology & Medicine
Yong-Hoon Kim, Jung Hwan Hwang, Jung-Ran Noh, Gil-Tae Gang, Do Hyung Kim, Hwa-Young Son, Tae Hwan Kwak, Minho Shong, In-Kyu Lee, Chul-Ho Lee
AIMS: Hypertension is one of the most common human diseases worldwide, and extensive research efforts are focused upon the identification and utilizing of novel therapeutic drug targets. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) is an important regulator of blood pressure (BP). β-Lapachone (βL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), increases the cellular NAD(+)/NADH ratio via the activation of NQO1. In this study, we evaluated whether βL-induced activation of NQO1 modulates BP in an animal model of hypertension...
August 1, 2011: Cardiovascular Research
Jung Hwan Hwang, Dong Wook Kim, Eun Jin Jo, Yong Kyung Kim, Young Suk Jo, Ji Hoon Park, Sang Ku Yoo, Myung Kyu Park, Tae Hwan Kwak, Young Lim Kho, Jin Han, Hueng-Sik Choi, Sang-Hee Lee, Jin Man Kim, InKyu Lee, Taeyoon Kyung, Cholsoon Jang, Jongkyeong Chung, Gi Ryang Kweon, Minho Shong
OBJECTIVE: Nicotinamide adenine dinucleotides (NAD+ and NADH) play a crucial role in cellular energy metabolism, and a dysregulated NAD+-to-NADH ratio is implicated in metabolic syndrome. However, it is still unknown whether a modulating intracellular NAD+-to-NADH ratio is beneficial in treating metabolic syndrome. We tried to determine whether pharmacological stimulation of NADH oxidation provides therapeutic effects in rodent models of metabolic syndrome. RESEARCH DESIGN AND METHODS: We used beta-lapachone (betaL), a natural substrate of NADH:quinone oxidoreductase 1 (NQO1), to stimulate NADH oxidation...
April 2009: Diabetes
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