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Objectives Reproductive malfunctions after chemotherapy still are a reason of reducing fertility and need specialized intensive care. The aim of this review was to investigate the effect of melatonin on the reproductive system under threatening with chemotherapeutic drugs. Methods To find the role of melatonin in the reproductive system during chemotherapy, a full systematic literature search was carried out based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines in the electronic databases up to 17 April 2017 using search terms in the titles and abstracts. A total of 380 articles are screened according to our inclusion and exclusion criteria. Finally, 18 articles were included in this study. Key findings It has been cleared that melatonin has bilateral effects on reproductive cells. Melatonin protects normal cells via mechanisms, including decrease in oxidative stress, apoptosis, inflammation and modulating mitochondrial function, and sexual hormones. Furthermore, melatonin with antiproliferative properties and direct effects on its receptors improves reproductive injury and function during chemotherapy. On the other hand, melatonin sensitizes the effects of chemotherapeutic drugs and enhances chemotherapy-induced toxicity in cancerous cells through increasing apoptosis, oxidative stress and mitochondrial malfunction. Conclusions The study provides evidence of the bilateral role of melatonin in the reproductive system during chemotherapy.

Aluminum phosphide (AlP), one of the most commonly used pesticides worldwide, has been the leading cause of self-poisoning mortalities among many Asian countries. The heart is the main organ affected in AlP poisoning. Melatonin has been previously shown to be beneficial in reversing toxic changes in the heart. The present study reveals evidence on the probable protective effects of melatonin on AlP-induced cardiotoxicity in rats. The study groups included a control (almond oil only), ethanol 5% (solvent), sole melatonin (50 mg/kg), AlP (16.7 mg/kg), and 4 AlP + melatonin groups which received 20, 30, 40 and 50 mg/kg of melatonin by intraperitoneal injections following AlP treatment. An electronic cardiovascular monitoring device was used to record the electrocardiographic (ECG) parameters. Heart tissues were studied in terms of oxidative stress biomarkers, mitochondrial complexes activities, ADP/ATP ratio and apoptosis. Abnormal ECG records as well as declined heart rate and blood pressure were found to be related to AlP administration. Based on the results, melatonin was highly effective in controlling AlP-induced changes in the study groups. Significant improvements were observed in the activities of mitochondrial complexes, oxidative stress biomarkers, the activities of caspases 3 and 9, and ADP/ATP ratio following treatment with melatonin at doses of 40 and 50 mg/kg. Our results indicate that melatonin can counteract the AlP-induced oxidative damage in the heart. This is mainly done by maintaining the normal balance of intracellular ATP as well as the prevention of oxidative damage. Further research is warranted to evaluate the possibility of using melatonin as an antidote in AlP poisoning.

Salient evidence testifies the link between organophosphorus (OPs) exposure and the formation of free radical oxidants; and it is well accepted that free radicals are one of the basic concerns of senescence. To show the oxidative features of phosalone (PLN) as a key member of OPs, to induce senescence in rat embryonic fibroblast (REF) cells and to demonstrate the beneficial effects of the known antioxidant ellagic acid (EA) in diminishing the PLN-induced toxic effects, the levels of cell viability, oxidative stress markers, inflammatory cytokines, telomerase activity, and the expression of the genes related to senescence were investigated. Our results lend support to the hypothesis that PLN enhances the entire premature senescence parameters of REF cells. This accounts for the mechanistic approval of the role of OPs in induction of senescence in rat fibroblasts. Moreover, incorporation of EA diminished PLN toxicity mainly through suppression of p38 and p53 at gene and protein levels, and tempered the inflammation factors (TNF-α, IL-1β, IL-6 and NF-κB), which further affected cell division. Analysis of cell cycle showed that the percentage of G0/G1 arrest, in REF cells treated by EA was elevated as compared to control and PLN treated cells.

BSTRACT Introduction: The aim of this study was to investigate the potential role of melatonin in the prevention of chemotherapy-induced nephrotoxicity at the preclinical level. Areas to be covered: To illuminate the possible role of melatonin in preventing chemotherapy-related nephrotoxicity, Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed. A comprehensive search strategy was developed to include PubMed, Web of Science, Scopus, and Embase electronic databases from their inception to May 2018. Based on a set of prespecified inclusion and exclusion criteria, 21 non-clinical articles were ultimately included in the study. Expert opinion: Our findings clearly demonstrate that melatonin has a protective role in the prevention of chemotherapy-induced nephrotoxicity which may be caused by different chemotherapy agents such as cyclophosphamide, cisplatin, doxorubicin, methotrexate, oxaliplatin, etoposide, and daunorubicin. On the basis of current review of non-clinical studies, this protective effect of melatonin is attributed to different mechanisms such as reduction of oxidative stress, apoptosis, and inflammation. The findings presented in this review are based on non-clinical studies and thus conducting appropriate clinical trials to evaluate the real effectiveness of the concurrent use of chemotherapy agents with melatonin in the cancer patients is necessary.

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