Melatonin enhances the developmental competence of porcine somatic cell nuclear transfer embryos by preventing DNA damage induced by oxidative stress

Liang, Shuang; Jin, Yong-Xun; Yuan, Bao; Zhang, Jiabao; Kim, Nam‐Hyung

doi:10.1038/s41598-017-11161-9

Cited by 49 publications

(43 citation statements)

References 69 publications

(76 reference statements)

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“…We observed a small improvement in Met + Mel group when compared to Met group, but it did not reach control values. The in vitro study done by Liang and colleagues (2017) showed that melatonin was able to attenuate the effect of oxidative stress and DNA damage on embryo cultures for fertilization. The antioxidant action of melatonin also improves fertility and maintains normal embryonic development, as observed in a review by Tamura et al (2012).…”

Section: Discussionmentioning

confidence: 99%

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Figueiró¹,

Moreira²,

Santos³

et al. 2019

Intl J of Devlp Neuroscience

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Elevated levels of methionine in blood characterize the hypermethioninemia, which may have genetic or non‐genetic origin, as for example from high protein diet. Born rats from hypermethioninemic mothers presented cerebral oxidative stress, inhibition of Na+,K+‐ATPase, memory deficit and ultrastructure cerebral changes. Melatonin is a hormone involved in circadian rhythm and has antioxidant effects. The aim of this study was to verify the possible neuroprotective effects of melatonin administration in hypermethioninemic pregnant rats on damage to biomolecules (Na+,K+‐ATPase, sulfhydryl content and DNA damage index) and behavior (open field, novel object recognition and water maze tasks), as well as its effect on cells morphology by electron microscopy in offspring. Wistar female rats received methionine (2.68 μmol/g body weight) and/or melatonin (10 mg/kg body weight) by subcutaneous injections during entire pregnancy. Control rats received saline. Biochemical analyzes were performed at 21 and 30 days of life of offspring and behavioral analyzes were performed only at 30 days of age in male pups. Results showed that gestational hypermethioninemia diminished Na+,K+‐ATPase activity and sulfhydryl content and increased DNA damage at 21 and 30 days of life. Melatonin was able to totally prevent Na+,K+‐ATPase activity alteration at 21 days and partially prevent its alteration at 30 days of rats life. Melatonin was unable in to prevent sulfhydryl and DNA damage at two ages. It also improved DNA damage, but not at level of saline animals (controls). Regarding to behavioral tests, data showed that pups exposed to gestational hypermethioninemia decreased reference memory in water maze, spent more time to the center of the open field and did not differentiate the objects in the recognition test. Melatonin was able to prevent the deficit in novel object recognition task. Electron microscopy revealed ultrastructure alterations in neurons of hypermethioninemic at both ages of offspring, whose were prevented by melatonin. These findings suggest that melatonin may be a good neuroprotective to minimize the harmful effects of gestational hypermethioninemia on offspring.

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Section: Discussionmentioning

confidence: 99%

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Figueiró¹,

Moreira²,

Santos³

et al. 2019

Intl J of Devlp Neuroscience

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“…Melatonin can easily penetrate the blood‐brain barrier, which allows it to control multiple physiological functions, such as insulin production and secretion, circadian rhythm, stress, mood, sleep, and sexual maturation . Although melatonin is well known as an endogenous circadian clock regulator, it also reduces drug‐induced free radical generation and exerts neuroprotective effects . A recent study found that melatonin enhances the oligodendrocyte differentiation of murine cortical neural stem cells .…”

Section: Introductionmentioning

confidence: 99%

Melatonin promotes neuroblastoma cell differentiation by activating hyaluronan synthase 3‐induced mitophagy

et al. 2019

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Neuroblastoma is the second most common pediatric malignancy and has a high rate of spontaneous remission. Uncovering the mechanisms underlying neuroblastoma cell differentiation is critical for therapeutic purposes. A neuroblastoma cell line (N2a) treated with either serum withdrawal (<2.5%) or melatonin (>0.1 nmol/L) for 24 hours was used as a cell differentiation research model. Interestingly, the hyaluronan synthase 3 (HAS3) protein was induced in differentiated N2a cells. N2a‐allografted nude mice received an intraperitoneal injection of melatonin (40 or 80 mg/kg/day for 3 weeks). The mean tumor volume in mice treated with 80 mg/kg melatonin was smaller than that in PBS‐treated mice (1416.3 and 3041.3 mm 3 , respectively, difference = 1625 mm 3 , * P = 0.0003, n = 7 per group). Compared with the vector control group, N2a cells with forced HAS3 overexpression showed significantly increased neuron length (* P = 0.00082) and neurite outgrowth (* P = 0.00059). Intracellular changes in autophagy, including distorted mitochondria with abnormal circular inner membranes, were detected by transmission electron microscopy (TEM). Our study demonstrated that HAS3‐mediated signaling activated by physiological concentrations of melatonin (>0.1 nmol/L) triggered significant N2a cell differentiation. These results provide molecular data with potential clinical relevance for therapeutic drug development.

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“…On the other hand, there is abundant evidence supporting the protective effects of melatonin against oxidative damage to DNA . The data gathered so far indicate that such protection is mediated by different pathways including both direct, that is, free radical scavenging processes, and indirect means of action. The latter may involve inhibiting metal‐induced oxidation, activating antioxidative enzymes, inhibiting pro‐oxidative enzymes, and/or enhancing the DNA repair machinery .…”

Section: Introductionmentioning

confidence: 99%

Melatonin and its metabolites as chemical agents capable of directly repairing oxidized DNA

Pérez-González

Castañeda‐Arriaga

Álvarez-Idaboy

et al. 2018

Journal of Pineal Research

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Oxidative stress mediates chemical damage to DNA yielding a wide variety of products. In this work, the potential capability of melatonin and several of its metabolites to repair directly (chemically) oxidative lesions in DNA was explored. It was found that all the investigated molecules are capable of repairing guanine‐centered radical cations by electron transfer at very high rates, that is, diffusion‐limited. They are also capable of repairing C‐centered radicals in the sugar moiety of 2′‐deoxyguanosine (2dG) by hydrogen atom transfer. Although this was identified as a rather slow process, with rate constants ranging from 1.75 to 5.32 × 102 M−1 s−1, it is expected to be fast enough to prevent propagation of the DNA damage. Melatonin metabolites 6‐hydroxymelatonin (6OHM) and 4‐hydroxymelatonin (4OHM) are also predicted to repair OH adducts in the imidazole ring. In particular, the rate constants corresponding to the repair of 8‐OH‐G adducts were found to be in the order of 104 M−1 s−1 and are assisted by a water molecule. The results presented here strongly suggest that the role of melatonin in preventing DNA damage might be mediated by its capability, combined with that of its metabolites, to directly repair oxidized sites in DNA through different chemical routes.

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Melatonin enhances the developmental competence of porcine somatic cell nuclear transfer embryos by preventing DNA damage induced by oxidative stress

Cited by 49 publications

References 69 publications

The neuroprotective role of melatonin in a gestational hypermethioninemia model

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Melatonin promotes neuroblastoma cell differentiation by activating hyaluronan synthase 3‐induced mitophagy

Melatonin and its metabolites as chemical agents capable of directly repairing oxidized DNA

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