Carbon monoxide releasing molecule A-1 attenuates acetaminophen-mediated hepatotoxicity and improves survival of mice by induction of Nrf2 and related genes

Upadhyay, Kapil; Jadeja, Ravirajsinh N.; Thadani, Jaymesh; Joshi, Apeksha; Vohra, Aliasgar; Mevada, Vishal; Patel, Rajesh; Khurana, Sandeep; Devkar, Ranjitsinh

doi:10.1016/j.taap.2018.09.034

Cited by 17 publications

(21 citation statements)

References 56 publications

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“…HO‐1 is an inducible enzyme that catalyzes the rate‐limiting step in the oxidative degradation of heme to free iron, biliverdin, and CO. 5‐ALA/SFC induces CO via HO‐1 induction, which is mediated by Nrf2 as reported previously . Furthermore, CO‐releasing molecules or CO gas induces HO‐1 expression via Nrf2 activation in vitro and in vivo . Therefore, suppression of HO‐1 expression may prevent CO release, thereby affecting 5‐ALA/SFC‐activated Nrf2 expression decline.…”

Section: Discussionsupporting

confidence: 67%

5‐ALA/SFC enhances HO‐1 expression through the MAPK/Nrf2 antioxidant pathway and attenuates murine tubular epithelial cell apoptosis

et al. 2019

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Cyclosporin A (CsA) is a common immunosuppressant, but its use is limited as it can cause chronic kidney injury. Oxidative stress and apoptosis play a key role in CsA‐induced nephrotoxicity. This study investigated the protective effect of 5‐aminolevulinic acid and iron (5‐ALA/SFC) on CsA‐induced injury in murine proximal tubular epithelial cells (mProx24). 5‐ALA/SFC significantly inhibited apoptosis in CsA‐treated mProx24 cells with increases in heme oxygenase (HO)‐1, nuclear factor E2‐related factor 2 (Nrf2), and p38, and Erk‐1/2 phosphorylation. Moreover, 5‐ALA/SFC suppressed production of reactive oxygen species in CsA‐exposed cells and inhibition of HO‐1 suppressed the protective effects of 5‐ALA/SFC. In summary, 5‐ALA/SFC may have potential for development into a treatment for the anti‐nephrotoxic/apoptotic effects of CsA.

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Section: Discussionsupporting

confidence: 67%

5‐ALA/SFC enhances HO‐1 expression through the MAPK/Nrf2 antioxidant pathway and attenuates murine tubular epithelial cell apoptosis

et al. 2019

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“…Therefore, this organ remains at the high risk of oxidative injury caused by the production of ROS. Oxidative stress has been considered a key factor causing liver damage induced by a variety of chemical and nonchemical agents, including alcohol, drugs, hepatic viral infections, and nutritional components, which in turn causes progression of hepatic injury, liver fibrosis, cirrhosis, and in some cases hepatocellular carcinoma [78][79][80][81]. These highly reactive species can be responsible for hepatic I/R injury occurring during surgical procedures such as liver resection and liver transplantation [82,83].…”

Section: Intestinal Mucosamentioning

confidence: 99%

“…This CO-induced protection was mainly manifested by suppressed lipid peroxidation, normalized GSH concentration, and SOD activity [91]. Furthermore, Upadhyay et al investigated the therapeutic potential of CORM-A1 in acetaminophen-(APAP-) induced liver injury in mice [79]. They showed elevated levels of serum transaminases, depleted hepatic GSH, and hepatocyte necrosis after APAP treatment [79].…”

Section: Alcoholic and Nonalcoholic Liver Damagementioning

confidence: 99%

“…Furthermore, Upadhyay et al investigated the therapeutic potential of CORM-A1 in acetaminophen-(APAP-) induced liver injury in mice [79]. They showed elevated levels of serum transaminases, depleted hepatic GSH, and hepatocyte necrosis after APAP treatment [79]. On the contrary, in mice injected with CORM-A1 after APAP administration, the reduction in serum transaminases, preservation of hepatic GSH, and attenuation of hepatocyte necrosis have been observed.…”

Section: Alcoholic and Nonalcoholic Liver Damagementioning

confidence: 99%

“…On the contrary, in mice injected with CORM-A1 after APAP administration, the reduction in serum transaminases, preservation of hepatic GSH, and attenuation of hepatocyte necrosis have been observed. Interestingly, mice that received a lethal dose of 7 Oxidative Medicine and Cellular Longevity APAP died but those cotreated with CORM-A1 showed a 50% survival [79]. Additionally, CORM-A1 prevented hepatic steatosis in high-fat high-fructose (HFHF) diet fed mice, used as a model of nonalcoholic steatohepatitis (NASH) [92].…”

Section: Alcoholic and Nonalcoholic Liver Damagementioning

confidence: 99%

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Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

Korbut

Brzozowski

Magierowski

2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress reflects an imbalance between oxidants and antioxidants in favor of the oxidants capable of evoking tissue damage. Like hydrogen sulfide (H2S) and nitric oxide (NO), carbon monoxide (CO) is an endogenous gaseous mediator recently implicated in the physiology of the gastrointestinal (GI) tract. CO is produced in mammalian tissues as a byproduct of heme degradation catalyzed by the heme oxygenase (HO) enzymes. Among the three enzymatic isoforms, heme oxygenase-1 (HO-1) is induced under conditions of oxidative stress or tissue injury and plays a beneficial role in the mechanism of protection against inflammation, ischemia/reperfusion (I/R), and many other injuries. According to recently published data, increased endogenous CO production by inducible HO-1, its delivery by novel pharmacological CO-releasing agents, or even the direct inhalation of CO has been considered a promising alternative in future experimental and clinical therapies against various GI disorders. However, the exact mechanisms underlying behind these CO-mediated beneficial actions are not fully explained and experimental as well as clinical studies on the mechanism of CO-induced protection are awaited. For instance, in a variety of experimental models related to gastric mucosal damage, HO-1/CO pathway and CO-releasing agents seem to prevent gastric damage mainly by reduction of lipid peroxidation and/or increased level of enzymatic antioxidants, such as superoxide dismutase (SOD) or glutathione peroxidase (GPx). Many studies have also revealed that HO-1/CO can serve as a potential defensive pathway against oxidative stress observed in the liver and pancreas. Moreover, increased CO levels after treatment with CO donors have been reported to protect the gut against formation of acute GI lesions mainly by the regulation of reactive oxygen species (ROS) production and the antioxidative activity. In this review, we focused on the role of H2S and NO molecular sibling, CO/HO pathway, and therapeutic potential of CO-releasing pharmacological tools in the regulation of oxidative stress-induced damage within the GI tract with a special emphasis on the esophagus, stomach, and intestines and also two solid and important metabolic abdominal organs, the liver and pancreas.

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CO as a Protective Mediator of Liver Injury

Joe¹,

Park²,

Do³

et al. 2022

Carbon Monoxide in Drug Discovery

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Carbon monoxide releasing molecule A-1 attenuates acetaminophen-mediated hepatotoxicity and improves survival of mice by induction of Nrf2 and related genes

Cited by 17 publications

References 56 publications

5‐ALA/SFC enhances HO‐1 expression through the MAPK/Nrf2 antioxidant pathway and attenuates murine tubular epithelial cell apoptosis

5‐ALA/SFC enhances HO‐1 expression through the MAPK/Nrf2 antioxidant pathway and attenuates murine tubular epithelial cell apoptosis

Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

CO as a Protective Mediator of Liver Injury

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