Melatonin and mitochondrial function

León, Josefa; Acuña-Castroviejo, Darı́o; Sainz, Rosa M.; Mayo, Juan C.; Tan, Dun Xian; Reíter, Russel J.

doi:10.1016/j.lfs.2004.03.003

Cited by 301 publications

(259 citation statements)

References 213 publications

(209 reference statements)

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“…2D). Since erythrocytes have the role to remove extracellular H 2 O 2 , 27,28) brain cells of hyperuricemic mice were likely to be susceptible to oxidative modification by H 2 O 2 , and actually the decrease in ATP synthesis reflects mitochondrial dysfunction. Therefore, it is possible that hyperuricemia and gout patients possess the risk of cerebral disorders resulting from the reduction of erythrocyte catalase activity.…”

Section: Resultsmentioning

confidence: 99%

Cerebral Oxidative Stress and Mitochondrial Dysfunction in Oxonate-Induced Hyperuricemic Mice

Watanabe

Kiyama

Sakamaki

et al. 2006

JOURNAL OF HEALTH SCIENCE

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Relation between blood uric acid levels and brain cell functions were examined using potassium oxonateinduced hyperuricemic mice and allopurinol-induced hypouricemic mice. In hyperuricemic mice and hypouricemic mice, erythrocyte catalase activity was significantly lower and higher, respectively, than that in the control group. No significant change of superoxide dismutase (SOD) activity or glutathione peroxidase activity was observed in either group. Cerebral lipid peroxide levels expressed as thiobarbituric acid reactive substances (TBARS) were significantly higher in hyperuricemic mice, and cerebral mitochondrial ATP synthesis and manganese-containing SOD (Mn-SOD) activity were significantly diminished in the same mice. In hypouricemic mice, no significant change was observed for TBARS levels, mitochondrial ATP synthesis and Mn-SOD activity. Then significant negative correlation between erythrocyte catalase activity and cerebral TBARS levels, and significant positive correlation between catalase activity and mitochondrial ATP synthesis were confirmed. Furthermore, when mouse erythrocytes were treated with uric acid, their catalase activities were particularly diminished. These results suggest that the reduction of erythrocyte catalase activity resulted from the elevation of blood uric acid levels is a major cause of cerebral oxidative stress and mitochondrial dysfunction in hyperuricemic mice. Therefore, it is possible that hyperuricemia and gout are risk factors of cerebral disorders.

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Section: Resultsmentioning

confidence: 99%

Cerebral Oxidative Stress and Mitochondrial Dysfunction in Oxonate-Induced Hyperuricemic Mice

Watanabe

Kiyama

Sakamaki

et al. 2006

JOURNAL OF HEALTH SCIENCE

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“…Com essa propriedade, a melatonina é capaz de eliminar os radicais livres gerados na mitocôndria, além de reduzir a fuga de elétrons a partir da cadeia respiratória, diminuindo a formação de EROs (Leon et al 2004). A melatonina, além de ser capaz de proteger as mitocôndrias dos danos oxidativos, reduzindo o consumo de oxigênio, é capaz de melhorar o potencial da membrana e a produção do ânion superóxido, mantendo, ao mesmo tempo, a produção de ATP (Lopez et al 2009).…”

Section: Discussionunclassified

Efeito de diferentes concentrações de melatonina em espermatozoides de carneiros sobre estresse oxidativo após criopreservação

et al. 2016

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ABSTRACT.-Souza W.L., Moraes E.A., Costa J.M.S., Souza P.H.F., Lopes Junior E.S., Oliveira R. The aim was to evaluate the effect of adding different concentrations of melatonin in ram semen diluted after cryopreservation. Ten ejaculates were collected0 from three adult ram (n=30) by means of artificial vagina for sheep. The collected samples were diluted in Tris-egg yolk, to a final concentration 200x10 6 sptz/mL kept in water bath at 32°C, and melatonin added as treatments: control; 100pM; 100nM; 100μM and 1mM melatonin. Then, the samples were cooled in a cold chamber at 5°C for two hours, in straws of 0.5mL and sealed. They were stored under the liquid nitrogen vapor for 15 minutes to 8cm of liquid blade and frozen with liquid nitrogen. Samples were analyzed for sperm motility, membrane integrity, acrosomal membrane, mitochondrial activity, oxidative stress and quantification of the binding capacity. The variables were subjected to analysis of variance and the means were compared by Tukey test at 5% probability. The total and progressive motility of thawed sperm were higher in samples treated with 100pM melatonin (62.99 and 45.07%, respectively; P<0.05) when compared to other treatments. The addition of different concentrations of melatonin in semen diluted with the exception of 1mM concentration, a higher percentage of cells with intact plasma membrane, as compared with the control (P<0.05). The percentage of sperm with acrosome membrane integrity was higher in the semen with 100pM melatonin (P<0.05) than the other treatments. The high mitochondrial activity was higher in spermatozoa treated with 100pM melatonin (69.30%; P<0.05). Addition of 100nM melatonin reduced the amount of TBARS after cryopreservation (2.84, P<0.05) when compared with the other treatments. After thawing, the number of sperm which bind to the perivitelline membrane was higher in the melatonin treated with 100pM (155,73; P<0.05). Therefore, melatonin addition the semen diluted can be useful to enhance the cryopreservation of sheep semen, improving fertilization rates through artificial insemination.

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“…Oxidative stresses increase and mitochondrial dysfunction are among pathophysiologic causes in neurodegenerative diseases such as Alzheimer, Parkinson and diabetes-induced peripheral neuropathy and the protective effect of melatonin in some of these neurodegenerative diseases has been proved (Tunez et al, 2003;Leon et al, 2004;Srinivasan, et al, 2006). Melatonin with regard to its various roles in relation to free radicals scavenging, regulation of oxidant and pro oxidant enzymes and also preventing the formation of mitochondrial radicals has a special importance in the treatment of neurodegenerative diseases (Srinivasan et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Effects of Melatonin in Prevention of Neuropathy in STZ-Induced Diabetic Rats

Zangiabadi¹,

Sheibani²,

Asadi-Shekaari³

et al. 2011

American Journal of Pharmacology and Toxicology

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Problem statement: Diabetes mellitus occurs mainly with chronic polyneuropathy, and oxidative stress plays an important role in emergence of most neurologic and behavioral changes in diabetic patients. Many studies have focused on the beneficial effects of various antioxidants such as melatonin on diabetic neuropathy. The aim of this study is to evaluate the effect of melatonin in prevention of neuropathy in Streptozotocin-induced diabetic rats. After prescribing Streptozotocin (STZ), treatment rats received melatonin (10 mg kg day −1 ) or DMSO for a period of 6 weeks. Approach: At the end of the sixth week, non diabetic control group, diabetic control group (sham) and treated rats were examined by thermal pain response tests (hot plate and tail flick). The horizontal and vertical activities of rats were measured in an open field test. After that, Motor Nerve Conduction Velocity (MNCV) of sciatic-tibial nerve recorded. Also, to study morphological alterations resulting from diabetic neuropathy of sciatic nerve, Myelinated Fiber Diameter (MFD), Axon Diameter (AD) and Myelin Sheath Diameter (MSD) were evaluated by light microscope. Results: According to hot plate results, response time to thermal pain at the end of sixth week in sham group showed a significant decrease in comparison with the control group (p<0.01). In hot plate test, although melatonin approximated to the response time to control group, the significant difference was not observed among melatonin receivers and other groups. In the open field test, Total Distance Moved (TDM) and mobility duration showed significant decrease in sham and DMSO groups in comparison to the control and melatonin groups. Diabetic rats treated with melatonin showed significant increase in MNCV compared to sham and DMSO groups (p<0.05). In morphological study, pretreatment with Melatonin significantly reversed sciatic nerve diameters (MFD, AD, and MSD) reduction in diabetic rats. Electron microscopy showed myelin splitting and myelin sheath infolding in diabetic control group compare to non diabetic group. Conclusion: This study showed that melatonin can decrease the destructive progress of diabetes and causes neuroprotection against damages resulting from STZinduced hyperglycemia.

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Melatonin and mitochondrial function

Cited by 301 publications

References 213 publications

Cerebral Oxidative Stress and Mitochondrial Dysfunction in Oxonate-Induced Hyperuricemic Mice

Cerebral Oxidative Stress and Mitochondrial Dysfunction in Oxonate-Induced Hyperuricemic Mice

Efeito de diferentes concentrações de melatonina em espermatozoides de carneiros sobre estresse oxidativo após criopreservação

Effects of Melatonin in Prevention of Neuropathy in STZ-Induced Diabetic Rats

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