A review of the protective effect of melatonin in pesticide-induced toxicity

Asghari, Mohammad Hossein; Moloudizargari, Milad; Bahadar, Haji; Abdollahi, Mohammad

doi:10.1080/17425255.2016.1214712

Cited by 54 publications

(26 citation statements)

References 77 publications

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“…As with ionizing radiation, these factors commonly induce injury by promoting the excessive generation of highly-destructive partially reduced oxygen species, i.e., ROS [100]. Some exogenous contributors to cellular DNA damage include environmental pollutants [101,102], exposure to heavy metals [103,104], toxic drugs [105,106], chemicals [107,108] (Figure 2), etc. Intracellularly, endogenous processes may also cause ROS production to the extent that it exceeds the capacity of the antioxidant defense network to fend off the damage associated with these oxygen metabolites.…”

Section: Cancer Initiation: Genomic Damage and Instabilitymentioning

confidence: 99%

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

Reíter

Rosales-Corral

Tan

et al. 2017

IJMS

358

368

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There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which melatonin reportedly restrains cancer development and growth. These diverse actions suggest that what is being observed are merely epiphenomena of an underlying more fundamental action of melatonin that remains to be disclosed. Some of the arresting actions of melatonin on cancer are clearly membrane receptor-mediated while others are membrane receptor-independent and involve direct intracellular actions of this ubiquitously-distributed molecule. While the emphasis of melatonin/cancer research has been on the role of the indoleamine in restraining breast cancer, this is changing quickly with many cancer types having been shown to be susceptible to inhibition by melatonin. There are several facets of this research which could have immediate applications at the clinical level. Many studies have shown that melatonin’s co-administration improves the sensitivity of cancers to inhibition by conventional drugs. Even more important are the findings that melatonin renders cancers previously totally resistant to treatment sensitive to these same therapies. Melatonin also inhibits molecular processes associated with metastasis by limiting the entrance of cancer cells into the vascular system and preventing them from establishing secondary growths at distant sites. This is of particular importance since cancer metastasis often significantly contributes to death of the patient. Another area that deserves additional consideration is related to the capacity of melatonin in reducing the toxic consequences of anti-cancer drugs while increasing their efficacy. Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level. Even if the only beneficial actions of melatonin in cancer patients are its ability to attenuate acute and long-term drug toxicity, melatonin should be used to improve the physical wellbeing of the patients. The experimental findings, however, suggest that the advantages of using melatonin as a co-treatment with conventional cancer therapies would far exceed improvements in the wellbeing of the patients.

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Section: Cancer Initiation: Genomic Damage and Instabilitymentioning

confidence: 99%

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

Reíter

Rosales-Corral

Tan

et al. 2017

IJMS

358

368

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“…Previous studies demonstrated that phosphine can trigger apoptosis pathways in several tissues such as heart, kidney and liver. [58] It was shown that AlP affects mitochondrial membrane fluidity leading to mitochondrial swelling and outer membrane rupture, thus resulting in the release of pro-apoptotic factors which in turn activates caspases to induce cell death. [38,59] The recent studies also confirmed the AlP-induced cardiomyocyte death through several pathways.…”

Section: Melatonin and Aluminium Phosphideinduced Apoptosismentioning

confidence: 99%

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

Asghari

Abdollahi

Oliveira

et al. 2016

Journal of Pharmacy and Pharmacology

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Objectives Acute poisoning with aluminium phosphide (AlP) is a major cause of mortality in developing countries. AlP mortality is due to cardiac dysfunction leading to cardiomyocyte death. The main mechanism is an inhibition of cytochrome c oxidase in the cardiomyocyte mitochondria, resulting in a decreased ATP production and oxidative stress. Unfortunately, the administration of exogenous drugs does not meet the desired requirements of an effective therapy. Melatonin is an amphiphilic molecule and can easily pass through all cellular compartments with the highest concentration recorded in mitochondria. It is known as a vigorous antioxidant, acting as a potent reactive oxygen species (ROS) scavenger. Our aim is to summarize the mechanisms by which melatonin may modulate the deteriorating effects of AlP poisoning on cardiac mitochondria. Key findings Melatonin not only mitigates the inhibition of respiratory chain complexes, but also increases ATP generation. Moreover, it can directly inhibit the mitochondrial permeability transition pore (mPTP) opening, thus preventing apoptosis. In addition, melatonin inhibits the release of cytochrome c from mitochondria to hinder caspase activation leading to cell survival. Summary Based on the promising effects of melatonin on mitochondria, melatonin may mitigate AlP-induced cardiotoxicity and might be potentially suggested as cardioprotective in AlP-intoxicated patients.

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“…The U.S. Dietary Supplement Health and Education Act of 1994 allow synthetic melatonin to be sold as a dietary supplement; there have not been any reported cases of proven toxicity or overdose by melatonin; in fact, melatonin was found to prevent the cytotoxic effects of other drugs (Asghari, et al 2016; Esteban-Zubero, et al 2016), including chemotherapeutic drugs (Demir, et al 2015). Clinical studies indicate a role for melatonin as an adjuvant therapy for sleep disorders of circadian etiology (jet lag, delayed sleep phase syndrome, sleep deterioration associated with aging, etc.)…”

Section: Regulation Of the Circadian Clock By Melatoninmentioning

confidence: 99%

WOMEN IN CANCER THEMATIC REVIEW: Circadian rhythmicity and the influence of ‘clock’ genes on prostate cancer

Kiss

Ghosh

2016

Endocrine-Related Cancer

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The androgen receptor (AR) plays a key role in the development and progression of prostate cancer (CaP). Since the mid-1990s, reports in the literature pointed out higher incidences of CaP in some select groups, such as airline pilots and night shift workers in comparison to those working regular hours. The common finding in these “high-risk” groups was that they all experienced a deregulation of the body’s internal circadian rhythm. Here we discuss how the circadian rhythm affects androgen levels and modulates CaP development and progression. Circadian rhythmicity of androgen production is lost in CaP patients, with the clock genes Per1 and Per2 decreasing, and Bmal1 increasing, in these individuals. Periodic expression of the clock genes was restored upon administration of the neurohormone melatonin, thereby suppressing CaP progression. Activation of the melatonin receptors and the AR antagonized each other, and therefore the tumor suppressive effects of melatonin and the clock genes were most clearly observed in the absence of androgens, that is, in conjunction with androgen deprivation therapy (ADT). In addition, a large-scale study found that high-dose radiation was more effective in CaP patients when it was delivered before 5PM, compared to those delivered after 5PM, suggesting that the therapy was more effective when delivered in synchrony with the patient’s circadian clock. As CaP patients are shown to become easily resistant to new therapies, perhaps circadian delivery of these therapeutic agents or delivery in conjunction with melatonin and its novel analogs should be tested to see if they prevent this resistance.

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A review of the protective effect of melatonin in pesticide-induced toxicity

Cited by 54 publications

References 77 publications

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

WOMEN IN CANCER THEMATIC REVIEW: Circadian rhythmicity and the influence of ‘clock’ genes on prostate cancer

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