Crosstalk between anticancer drugs and mitochondrial functions

Sahu, Kuleshwar; Langeh, Urvashi; Singh, Charan; Singh, Arti

doi:10.1016/j.crphar.2021.100047

Cited by 28 publications

(16 citation statements)

References 126 publications

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“…In contrast, toxic properties, particularly doses of mitochondrial-mediated programmed cell death, affect not only cancer cells or parasitic cells but also normal host cells. It has been reported that chemotherapeutic drugs can cause collateral damage to normal cells, such as the occurrence of chemobrain or CICI (chemotherapy-induced cognitive impairment) due to mitochondrial dysfunction and oxidative stress [ 18 ]. Therefore, the risk/benefit ratio of the administration of drugs, chemicals, and pharmaceuticals should be considered and balanced.…”

Section: Discussionmentioning

confidence: 99%

High-Dose Primaquine Induces Proximal Tubular Degeneration and Ventricular Cardiomyopathy Linked to Host Cells Mitochondrial Dysregulation

Rabiablok

Hanboonkunupakarn

Tuentam

et al. 2023

Toxics

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Primaquine (PQ) is the only antimalarial medication used to eradicate many species of Plasmodium gametocytes and prevent relapse in vivax and ovale malarias. PQ metabolites induce oxidative stress and impair parasitic mitochondria, leading to protozoal growth retardation and death. Collateral damage is also presented in mammalian host cells, particularly erythrocytes, resulting in hemolysis and tissue destruction. However, the underlying mechanisms of these complications, particularly the mitochondria-mediated cell death of the host, are poorly understood. In the present study, toxicopathological studies were conducted on a rat model to determine the effect of PQ on affected tissues and mitochondrial toxicity. The results indicated that the LD50 for PQ is 200 mg/kg. A high dose of PQ induced hemolytic anemia, elevated a hepatic enzyme (SGPT), and induced proximal tubular degeneration, ventricular cardiomyopathy, and mitochondrial dysregulation. In addition, PQ induced the upregulation of apoptosis-related proteins Drp-1 and caspase-3, with a positive correlation, as well as the pro-apoptotic mitochondrial gene expression of Bax, reflecting the toxic effect of high doses of PQ on cellular damage and mitochondrial apoptosis in terms of hepatotoxicity, nephrotoxicity, and cardiotoxicity. Regarding the risk/benefit ratio of drug administration, our research provides caution for the use of PQ in the treatment of malaria based on its toxicopathological effects.

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Section: Discussionmentioning

confidence: 99%

High-Dose Primaquine Induces Proximal Tubular Degeneration and Ventricular Cardiomyopathy Linked to Host Cells Mitochondrial Dysregulation

Rabiablok

Hanboonkunupakarn

Tuentam

et al. 2023

Toxics

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“… 6 Among them, mitochondrial dysfunction is reported to be significant pathogenesis of CIPN, which corresponds to the clinical manifestations. 11 – 15 …”

Section: Mitochondrial Dysfunction In Cipnmentioning

confidence: 99%

PGC1α: an emerging therapeutic target for chemotherapy-induced peripheral neuropathy

Zhai

Zheng

et al. 2023

Ther Adv Neurol Disord

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Chemotherapy-induced peripheral neuropathy (CIPN)-mediated paresthesias are a common complication in cancer patients undergoing chemotherapy. There are currently no treatments available to prevent or reverse CIPN. Therefore, new therapeutic targets are urgently needed to develop more effective analgesics. However, the pathogenesis of CIPN remains unclear, and the prevention and treatment strategies of CIPN are still unresolved issues in medicine. More and more studies have demonstrated that mitochondrial dysfunction has become a major factor in promoting the development and maintenance of CIPN, and peroxisome proliferator-activated receptor gamma (PPARγ) coactivator 1α (PGC1α) plays a significant role in maintaining the mitochondrial function, protecting peripheral nerves, and alleviating CIPN. In this review, we highlight the core role of PGC1α in regulating oxidative stress and maintaining normal mitochondrial function and summarize recent advances in its therapeutic effects and mechanisms in CIPN and other forms of peripheral neuropathy. Emerging studies suggest that PGC1α activation may positively impact CIPN mitigation by modulating oxidative stress, mitochondrial dysfunction, and inflammation. Therefore, novel therapeutic strategies targeting PGC1α could be a potential therapeutic target in CIPN.

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“…After ionizing radiation, persistent oxidative stress characterized by mitochondrial dysfunction and upregulation of the NADPH oxidase complex is observed [173]. Likewise, chemotherapeutic drugs such as platinum-based drugs, adriamycin, and cyclophosphamide, impair the normal mitochondrial function and antioxidant response that increases superoxide anion [174].…”

Section: Oncologymentioning

confidence: 99%

Modulating the Antioxidant Response for Better Oxidative Stress-Inducing Therapies: How to Take Advantage of Two Sides of the Same Medal?

et al. 2022

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Oxidative stress-inducing therapies are characterized as a specific treatment that involves the production of reactive oxygen and nitrogen species (RONS) by external or internal sources. To protect cells against oxidative stress, cells have evolved a strong antioxidant defense system to either prevent RONS formation or scavenge them. The maintenance of the redox balance ensures signal transduction, development, cell proliferation, regulation of the mechanisms of cell death, among others. Oxidative stress can beneficially be used to treat several diseases such as neurodegenerative disorders, heart disease, cancer, and other diseases by regulating the antioxidant system. Understanding the mechanisms of various endogenous antioxidant systems can increase the therapeutic efficacy of oxidative stress-based therapies, leading to clinical success in medical treatment. This review deals with the recent novel findings of various cellular endogenous antioxidant responses behind oxidative stress, highlighting their implication in various human diseases, such as ulcers, skin pathologies, oncology, and viral infections such as SARS-CoV-2.

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Crosstalk between anticancer drugs and mitochondrial functions

Cited by 28 publications

References 126 publications

High-Dose Primaquine Induces Proximal Tubular Degeneration and Ventricular Cardiomyopathy Linked to Host Cells Mitochondrial Dysregulation

High-Dose Primaquine Induces Proximal Tubular Degeneration and Ventricular Cardiomyopathy Linked to Host Cells Mitochondrial Dysregulation

PGC1α: an emerging therapeutic target for chemotherapy-induced peripheral neuropathy

Modulating the Antioxidant Response for Better Oxidative Stress-Inducing Therapies: How to Take Advantage of Two Sides of the Same Medal?

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