Melatonin effect on the ultrastructure of Ehrlich ascites tumor cells, lifetime and histopathology in Swiss mice

Batista, Ana Paula Castor; Silva, Terezinha G. da; Teixeira, Álvaro A.C.; Medeiros, Paloma Lys de; Teixeira, Valéria Wanderley; Alves, Luíz Carlos; Santos, Fábio André Brayner dos

doi:10.1016/j.lfs.2013.10.012

Cited by 13 publications

(11 citation statements)

References 48 publications

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“…It is in fact documented how the induction of cellular death in cancer cells is mostly active at pharmacological doses; this has been stressed in several cellular lines and in vivo [ 38 , 39 , 48 , 49 ]. On the contrary, at low doses it can even improve the vitality in many cytotypes, also neoplastic, or appear totally inactive (or active only in some neoplastic forms); it can even exert only an oncostatic effect.…”

Section: Discussionmentioning

confidence: 99%

Oncostatic-Cytoprotective Effect of Melatonin and Other Bioactive Molecules: A Common Target in Mitochondrial Respiration

Pacini¹,

Borziani²

2016

IJMS

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For several years, oncostatic and antiproliferative properties, as well as thoses of cell death induction through 5-methoxy-N-acetiltryptamine or melatonin treatment, have been known. Paradoxically, its remarkable scavenger, cytoprotective and anti-apoptotic characteristics in neurodegeneration models, such as Alzheimer’s disease and Parkinson’s disease are known too. Analogous results have been confirmed by a large literature to be associated to the use of many other bioactive molecules such as resveratrol, tocopherol derivatives or vitamin E and others. It is interesting to note that the two opposite situations, namely the neoplastic pathology and the neurodegeneration, are characterized by deep alterations of the metabolome, of mitochondrial function and of oxygen consumption, so that the oncostatic and cytoprotective action can find a potential rationalization because of the different metabolic and mitochondrial situations, and in the effect that these molecules exercise on the mitochondrial function. In this review we discuss historical and general aspects of melatonin, relations between cancers and the metabolome and between neurodegeneration and the metabolome, and the possible effects of melatonin and of other bioactive molecules on metabolic and mitochondrial dynamics. Finally, we suggest a common general mechanism as responsible for the oncostatic/cytoprotective effect of melatonin and of other molecules examined.

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Section: Discussionmentioning

confidence: 99%

Oncostatic-Cytoprotective Effect of Melatonin and Other Bioactive Molecules: A Common Target in Mitochondrial Respiration

Pacini¹,

Borziani²

2016

IJMS

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“…Another study showed that melatonin was able to induce cell death on a human alveolar rhabdomyosarcoma cell line in a dose- and time-dependent manner [181]. Furthermore, melatonin treatment at 150 and 300 μg/30 g bw for 12 consecutive days could induce a very effective oncostatic and cytotoxic activity in mice incubated with Ehrlich ascites tumor cells [182]. …”

Section: Experimental Studiesmentioning

confidence: 99%

Melatonin for the prevention and treatment of cancer

et al. 2017

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The epidemiological studies have indicated a possible oncostatic property of melatonin on different types of tumors. Besides, experimental studies have documented that melatonin could exert growth inhibition on some human tumor cells in vitro and in animal models. The underlying mechanisms include antioxidant activity, modulation of melatonin receptors MT1 and MT2, stimulation of apoptosis, regulation of pro-survival signaling and tumor metabolism, inhibition on angiogenesis, metastasis, and induction of epigenetic alteration. Melatonin could also be utilized as adjuvant of cancer therapies, through reinforcing the therapeutic effects and reducing the side effects of chemotherapies or radiation. Melatonin could be an excellent candidate for the prevention and treatment of several cancers, such as breast cancer, prostate cancer, gastric cancer and colorectal cancer. This review summarized the anticancer efficacy of melatonin, based on the results of epidemiological,experimental and clinical studies, and special attention was paid to the mechanisms of action.

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“…Mel has been described as a molecule with remarkable pro-apoptotic activity in many tumor types, such as Ehrlich tumor, colorectal, breast, and liver (Cos et al 2002, Batista et al 2013, Fan et al 2013, Hong et al 2014. Activities of Mel on such tumors include modulation of BAX and Bcl-2 (Hong et al 2014), p53 and p21 (Cos et al 2002), and further regulation of caspase-3 with the release of cytochrome c (Perdomo et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

Chuffa¹,

Alves²,

Martinez³

et al. 2015

Endocrine-Related Cancer

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Apoptosis plays an important role in the treatment of cancer, and targeting apoptosis-related molecules in ovarian cancer (OC) is of great therapeutic value. Melatonin (Mel) is an indoleamine displaying several anti-cancer properties and has been reported to modulate apoptosis signaling in multiple tumor subtypes. We investigated OC and the role of Mel therapy on the pro-apoptotic (p53, BAX, caspase-3, and cleaved caspase-3) and anti-apoptotic (Bcl-2 and survivin) proteins in an ethanol (EtOH)-preferring rat model. To induce OC, the left ovary was injected directly with a single dose of 100 mg 7,12-dimethylbenz(a)anthracene dissolved in 10 ml of sesame oil under the bursa. Right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of Mel (200 mg/100 g BW per day) for 60 days. Body weight gain, EtOH consumption, and energy intake were unaffected by the treatments. Interestingly, absolute and relative OC masses showed a significant reduction after Mel therapy, regardless of EtOH consumption. To accomplish OC-related apoptosis, we first observed that p53, BAX, caspase-3, and cleaved caspase-3 were downregulated in OC tissue while Bcl-2 and survivin were overexpressed. Notably, Mel therapy and EtOH intake promoted apoptosis along with the upregulation of p53, BAX, and cleaved caspase-3. Fragmentation of DNA observed by TUNEL-positive nuclei was also enhanced following Mel treatment. In addition, Bcl-2 was downregulated by the EtOH intake and lower survivin levels were observed after Mel therapy. Taken together, these results suggest that Mel induce apoptosis in OC cells of EtOH-preferring animals.Key Words " ovarian cancer " melatonin " pro-apoptotic protein " anti-apoptotic protein

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Melatonin effect on the ultrastructure of Ehrlich ascites tumor cells, lifetime and histopathology in Swiss mice

Cited by 13 publications

References 48 publications

Oncostatic-Cytoprotective Effect of Melatonin and Other Bioactive Molecules: A Common Target in Mitochondrial Respiration

Oncostatic-Cytoprotective Effect of Melatonin and Other Bioactive Molecules: A Common Target in Mitochondrial Respiration

Melatonin for the prevention and treatment of cancer

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

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