Studies on curative efficacy of monoterpene eugenol on anti- leukemic drug arsenic trioxide induced cardiotoxicity

Binu, Prakash; Priya, N.; Abhilash, S; Vineetha, Radhakrishnan Chandraprabha; Nair, R. Harikumaran

doi:10.1016/j.biopha.2017.04.087

Cited by 32 publications

(29 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, Binu et al [28] showed that eugenol restored liver function from arsenic-induced liver injury. Further, the antioxidant effects of eugenol have been highlighted in various disease models, proving its versatility [29,30].…”

Section: Discussionmentioning

confidence: 99%

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Liu

Mao

2019

Arch biol sci (Beogr)

View full text Add to dashboard Cite

Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

show abstract

Section: Discussionmentioning

confidence: 99%

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Liu

Mao

2019

Arch biol sci (Beogr)

View full text Add to dashboard Cite

show abstract

“…Oxidized glutathione can be converted back to its reduced state using NADPH as an electron donor, and the ratio of GSH/GSSG is often used as a measure of oxidative stress [ 31 ]. Glutathione S-transferase (GST) utilizes GSH as a substrate and participates in the metabolism of xenobiotics [ 32 ], and glutathione peroxidase (GPx) and thioredoxin reductase (TR) catalyze interconversion and equilibrium among reduced/oxidized species [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

“…Arsenic is considered a “sulfhydryl-reactive metalloid” [ 35 ]. The affinity of arsenic for free sulfhydryl groups results in certain mechanisms of toxicity, including binding and depletion of GSH pools, as well as binding and inactivation of sulfhydryl-rich proteins [ 32 ]. This cysteine thiol binding-mediated inactivation of specific proteins is central to the ability of arsenic to both induce metallothionein biosynthesis [ 36 ] and elevate ROS generation via inhibition of the antioxidant enzyme thioredoxin reductase [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…As previously noted, GSH is also consumed during metabolism of arsenic and in response to arsenic-induced ROS. Indeed, GST utilizes GSH as a substrate and participates in the xenobiotic metabolism of arsenic and other compounds [ 32 ] and GPx catalyzes the reduction of H 2 O 2 to H 2 O with GSH as a substrate [ 32 , 48 ]. Furthermore, decreased availability of GSH due to arsenic toxicity further contributes to ROS accumulation [ 49 ].…”

Section: Introductionmentioning

confidence: 99%

“…In this process, free radicals cause cell damage by sequestering electrons from the lipids in cell membranes [ 50 ]. Additionally, arsenic may decrease membrane-based enzyme activity through the generation of ROS [ 32 ]. For instance, ROS inhibit the activity of Na + /K + ATPase resting membrane homeostasis, which is critical for maintaining mitochondrial transmembrane potential [ 51 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Antioxidants Protect against Arsenic Induced Mitochondrial Cardio-Toxicity

Pace

Dagda

Angermann

2017

Toxics

View full text Add to dashboard Cite

Arsenic is a potent cardiovascular toxicant associated with numerous biomarkers of cardiovascular diseases in exposed human populations. Arsenic is also a carcinogen, yet arsenic trioxide is used as a therapeutic agent in the treatment of acute promyelotic leukemia (APL). The therapeutic use of arsenic is limited due to its severe cardiovascular side effects. Many of the toxic effects of arsenic are mediated by mitochondrial dysfunction and related to arsenic’s effect on oxidative stress. Therefore, we investigated the effectiveness of antioxidants against arsenic induced cardiovascular dysfunction. A growing body of evidence suggests that antioxidant phytonutrients may ameliorate the toxic effects of arsenic on mitochondria by scavenging free radicals. This review identifies 21 antioxidants that can effectively reverse mitochondrial dysfunction and oxidative stress in cardiovascular cells and tissues. In addition, we propose that antioxidants have the potential to improve the cardiovascular health of millions of people chronically exposed to elevated arsenic concentrations through contaminated water supplies or used to treat certain types of leukemias. Importantly, we identify conceptual gaps in research and development of new mito-protective antioxidants and suggest avenues for future research to improve bioavailability of antioxidants and distribution to target tissues in order reduce arsenic-induced cardiovascular toxicity in a real-world context.

show abstract

Arsenic trioxide: applications, mechanisms of action, toxicity and rescue strategies to date

Yan,

Wang,

Wei

et al. 2023

Arch. Pharm. Res.

View full text Add to dashboard Cite

Studies on curative efficacy of monoterpene eugenol on anti- leukemic drug arsenic trioxide induced cardiotoxicity

Cited by 32 publications

References 43 publications

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Antioxidants Protect against Arsenic Induced Mitochondrial Cardio-Toxicity

Arsenic trioxide: applications, mechanisms of action, toxicity and rescue strategies to date

Contact Info

Product

Resources

About