Long-term melatonin treatment delays ovarian aging

2017 ◽  
Vol 62 (2) ◽  
pp. e12381 ◽  
Author(s):  
Hiroshi Tamura ◽  
Mai Kawamoto ◽  
Shun Sato ◽  
Isao Tamura ◽  
Ryo Maekawa ◽  
...  
Keyword(s):  
Melatonin Treatment ◽  
Treatment Delays ◽  
Ovarian Aging

scholarly journals Melatonin administration prevents cardiac and diaphragmatic mitochondrial oxidative damage in senescence-accelerated mice

2007 ◽  
Vol 194 (3) ◽  
pp. 637-643 ◽  
Author(s):  
M I Rodriguez ◽  
G Escames ◽  
L C López ◽  
J A García ◽  
F Ortiz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Chronic Treatment ◽  
Melatonin Treatment ◽  
Mitochondrial Oxidative Stress ◽  
Melatonin Administration ◽  
Age Dependent ◽  
Mitochondrial Oxidative Damage ◽  
Senescence Accelerated Mice ◽  
Ratio Reduction

Cardiac and diaphragmatic mitochondria from male SAMP8 (senescent) and SAMR1 (resistant) mice of 5 or 10 months of age were studied. Levels of lipid peroxidation (LPO), glutathione (GSH), GSH disulfide (GSSG), and GSH peroxidase and GSH reductase (GRd) activities were measured. In addition, the effect of chronic treatment with the antioxidant melatonin from 1 to 10 months of age was evaluated. Cardiac and diaphragmatic mitochondria show an age-dependent increase in LPO levels and a reduction in GSH:GSSG ratios. Chronic treatment with melatonin counteracted the age-dependent LPO increase and GSH:GSSG ratio reduction in these mitochondria. Melatonin also increased GRd activity, an effect that may account for the maintenance of the mitochondrial GSH pool. Total mitochondrial content of GSH increased after melatonin treatment. In general, the effects of age and melatonin treatment were similar in senescence-resistant mice (SAMR1) and SAMP8 cardiac and diaphragmatic mitochondria, suggesting that these mice strains display similar mitochondrial oxidative damage at the age of 10 months. The results also support the efficacy of long-term melatonin treatment in preventing the age-dependent mitochondrial oxidative stress.

Influence of melatonin and oestradiol on the opioidergic regulation of LH and prolactin release in pony mares

1997 ◽  
Vol 154 (2) ◽  
pp. 241-248 ◽  
Author(s):  
C Aurich ◽  
J Lange ◽  
H-O Hoppen ◽  
J E Aurich
Keyword(s):  
Prolactin Secretion ◽  
Opioid Antagonist ◽  
Short Term ◽  
Melatonin Treatment ◽  
Prolactin Release ◽  
Oestradiol Treatment ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

Abstract The aim of this study was to investigate the influence of oestradiol, melatonin and season on the opioid regulation of LH and prolactin release. Effects of the opioid antagonist naloxone (0·5 mg/kg) on LH and prolactin secretion were determined in ovariectomized pony mares. In experiment 1, mares in January (n=6) were pretreated with oestradiol benzoate (5 μg/kg) for 20 days. In experiment 2, beginning in May, mares (n=7) received melatonin (15 mg) for 15 days and subsequently a combination of melatonin plus oestradiol for 20 days. In experiment 3, beginning in May, mares (n=6) were pretreated with oestradiol for 30 days, left untreated for 12 days and then given melatonin for 35 days. In all experiments the animals were injected with the opioid antagonist naloxone and saline on 2 consecutive days prior to treatment. In experiment 1, animals received naloxone and saline on days 10 and 11 and 20 and 21 following oestradiol treatment. In experiment 2, naloxone and saline were administered on days 15 and 16 following melatonin treatment and on days 10 and 11 and 20 and 21 of melatonin plus oestradiol treatment. In experiment 3, the animals received naloxone and saline on days 10 and 11, 20 and 21 and 30 and 31 of oestradiol treatment, prior to melatonin treatment and on days 15 and 16, 25 and 26 and 35 and 36 following melatonin. In January (experiment 1), naloxone evoked a significant (P<0·05) LH release at all times, however the LH increment in response to naloxone increased during oestradiol pretreatment (P<0·05) During the breeding season (experiments 2 and 3), naloxone induced a significant (P<0·05) increase in plasma LH concentrations when mares had not been pretreated with oestradiol or melatonin and after oestradiol pretreatment. Basal LH concentrations and the LH increment in response to naloxone increased significantly (P<0·05) during the 30-day oestradiol pretreatment. Melatonin decreased the naloxone-induced LH release and the LH release in response to naloxone and saline no longer differed after 25 and 35 days of melatonin pretreatment. When melatonin was given together with oestradiol for 20 days, again a significant (P<0·05) LH release in response to naloxone occurred. Prolactin release was significantly (P<0·05) increased by naloxone when mares had been pretreated with only melatonin. The opioid antagonist did not affect prolactin release in mares that had not been pretreated or received oestradiol either alone or in combination with melatonin. In conclusion, in long-term ovariectomized mares, opioids inhibit LH secretion independent from ovarian factors. This opioid inhibition of LH secretion is enhanced by oestradiol and reduced by melatonin. Although short-term melatonin treatment in-activates the opioid regulation of LH release, a prolonged influence of melatonin as occurs in winter does not prevent activation of the opioid system. This indicates that effects of melatonin on the opioid regulation of LH release change with time. An opioid inhibition of prolactin secretion is activated by melatonin given for 15–35 days but is lost under the prolonged influence of a short-day melatonin signal in winter. Journal of Endocrinology (1997) 154, 241–248

Long-term evaluation of cytoarchitectonic characteristics of prefrontal cortex pyramidal neurons, following global cerebral ischemia and neuroprotective melatonin treatment, in rats

2008 ◽  
Vol 448 (1) ◽  
pp. 148-152 ◽  
Author(s):  
Dafne García-Chávez ◽  
Ignacio González-Burgos ◽  
Graciela Letechipía-Vallejo ◽  
Elisa López-Loeza ◽  
Gabriela Moralí ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Cerebral Ischemia ◽  
Pyramidal Neurons ◽  
Global Cerebral Ischemia ◽  
Melatonin Treatment ◽  
Term Evaluation

Long-term exendin-4 treatment delays natural deterioration of glycaemic control in diabetic Goto-Kakizaki rats

2009 ◽  
Vol 11 (9) ◽  
pp. 884-890 ◽  
Author(s):  
L. Simonsen ◽  
S. Pilgaard ◽  
C. Orskov ◽  
B. Hartmann ◽  
J. J. Holst ◽  
...  
Keyword(s):  
Glycaemic Control ◽  
Treatment Delays

scholarly journals Characterization of Chemically Induced Ovarian Carcinomas in an Ethanol-Preferring Rat Model: Influence of Long-Term Melatonin Treatment

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e81676 ◽  
Author(s):  
Luiz Gustavo A. Chuffa ◽  
Beatriz A. Fioruci-Fontanelli ◽  
Leonardo O. Mendes ◽  
Wagner J. Fávaro ◽  
Patricia Fernanda F. Pinheiro ◽  
...  
Keyword(s):  
Rat Model ◽  
Ovarian Carcinomas ◽  
Melatonin Treatment ◽  
Chemically Induced

scholarly journals Long term melatonin treatment is safe in children with Down syndrome

2020 ◽  
Vol 49 (1) ◽  
pp. 8-12
Author(s):  
Nesreen K yasien ◽  
Mohamed A Abdraboh ◽  
Mohammed Al-haggar ◽  
Nehad Nasef ◽  
Mohamed A El-Missiry
Keyword(s):  
Down Syndrome ◽  
Melatonin Treatment ◽  
Children With Down Syndrome

scholarly journals Crisis management in the treatment of childhood acute lymphoblastic leukemia: putting right what can go wrong (emergency complications of disease and treatment)

Hematology ◽  
2017 ◽  
Vol 2017 (1) ◽  
pp. 251-258 ◽  
Author(s):  
Rachael Hough ◽  
Ajay Vora
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Tumor Lysis Syndrome ◽  
Treatment Delays ◽  
Life Threatening ◽  
Pediatric All ◽  
Short And Long Term ◽  
Dose Reductions ◽  
Related Mortality

AbstractThe improvement in overall survival in children with acute lymphoblastic leukemia (ALL) over the last 5 decades has been considerable, with around 90% now surviving long term. The risk of relapse has been reduced to such an extent that the risk of treatment-related mortality is now approaching that of mortality caused by relapse. Toxicities may also lead to the suboptimal delivery of chemotherapy (treatment delays, dose reductions, dose omissions), potentially increasing relapse risk, and short- and long-term morbidity, adding to the “burden of therapy” in an increasing number of survivors. Thus, the need to reduce toxicity in pediatric ALL is becoming increasingly important. This work focuses on the risk factors, pathogenesis, clinical features, and emergency management of the life-threatening complications of ALL at presentation and during subsequent chemotherapy, including leucostasis, tumor lysis syndrome, infection, methotrexate encephalopathy, thrombosis, and pancreatitis. Potential strategies to abrogate these toxicities in the future are also discussed.

scholarly journals Long-Term Dabigatran Treatment Delays Alzheimer’s Disease Pathogenesis in the TgCRND8 Mouse Model

2019 ◽  
Vol 74 (15) ◽  
pp. 1910-1923 ◽  
Author(s):  
Marta Cortes-Canteli ◽  
Anna Kruyer ◽  
Irene Fernandez-Nueda ◽  
Ana Marcos-Diaz ◽  
Carlos Ceron ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Disease Pathogenesis ◽  
Treatment Delays ◽  
Tgcrnd8 Mouse
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