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Bharti V.K.,Indian Veterinary Research Institute | Bharti V.K.,Defence Institute of High Altitude Research DIHAR | Srivastava R.S.,Indian Veterinary Research Institute | Kumar H.,Indian Veterinary Research Institute | And 5 more authors.
Advances in Pharmacological Sciences | Year: 2014

Several experimental and clinical reports indicated the oxidative stress-mediated adverse changes in vital organs of human and animal in fluoride (F) toxicity. Therefore, the present study was undertaken to evaluate the therapeutic effect of buffalo (Bubalus bubalis) epiphyseal (pineal) proteins (BEP) and melatonin (MEL) against F-induced oxidative stress in heart, liver, and kidney of experimental adult female rats. To accomplish this experimental objective, twenty-four adult female Wistar rats (123-143 g body weights) were divided into four groups, namely, control, F, F + BEP, and F + MEL and were administered sodium fluoride (NaF, 150 ppm elemental F in drinking water), MEL (10 mg/kg BW, i.p.), and BEP (100 μg/kg BW, i.p.) for 28 days. There were significantly P < 0.05 high levels of lipid peroxidation and catalase and low levels of reduced glutathione, superoxide dismutase, glutathione reductase, and glutathione peroxidase in cardiac, hepatic, and renal tissues of F-treated rats. Administration of BEP and MEL in F-treated rats, however, significantly P < 0.05 attenuated these adverse changes in all the target components of antioxidant defense system of cardiac, hepatic, and renal tissues. The present data suggest that F can induce oxidative stress in liver, heart, and kidney of female rats which may be a mechanism in F toxicity and these adverse effects can be ameliorated by buffalo (Bubalus bubalis) epiphyseal proteins and melatonin by upregulation of antioxidant defense system of heart, liver, and kidney of rats. © 2014 Vijay K. Bharti et al.

Srinivasan V.,Sri Sathya Sai Medical Educational and Research Foundation | Cardinali D.P.,Pontifical Catholic University of Argentina | Srinivasan U.S.,MIOT Hospital | Kaur C.,National University of Singapore | And 4 more authors.
Therapeutic Advances in Neurological Disorders | Year: 2011

Sleep disorders constitute major nonmotor features of Parkinson's disease (PD) that have a substantial effect on patients' quality of life and can be related to the progression of the neurodegenerative disease. They can also serve as preclinical markers for PD, as it is the case for rapid eye movement (REM)-associated sleep behavior disorder (RBD). Although the etiology of sleep disorders in PD remains undefined, the assessment of the components of the circadian system, including melatonin secretion, could give therapeutically valuable insight on their pathophysiopathology. Melatonin is a regulator of the sleep/wake cycle and also acts as an effective antioxidant and mitochondrial function protector. A reduction in the expression of melatonin MT1 and MT2 receptors has been documented in the substantia nigra of PD patients. The efficacy of melatonin for preventing neuronal cell death and for ameliorating PD symptoms has been demonstrated in animal models of PD employing neurotoxins. A small number of controlled trials indicate that melatonin is useful in treating disturbed sleep in PD, in particular RBD. Whether melatonin and the recently developed melatonergic agents (ramelteon, tasimelteon, agomelatine) have therapeutic potential in PD is also discussed. © The Author(s), 2011. Reprints and permissions: http://www.sagepub.co.uk/journalsPermissions.nav.

Srinivasan V.,Educational and Research Foundation | Spence D.W.,323 Brock Avenue | Pandi-Perumal S.R.,Somnogen Inc. | Brown G.M.,Center for Addiction and Mental Health | Cardinali D.P.,University of Buenos Aires
International Journal of Alzheimer's Disease | Year: 2011

Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R. Copyright 2011 Venkatramanujam Srinivasan et al.

Pandi-Perumal S.R.,Somnogen Inc. | Kramer M.,University of Illinois at Chicago
Sleep and Mental Illness | Year: 2010

The diagnosis of mental illness is frequently accompanied by sleep problems; conversely, people experiencing sleep problems may subsequently develop mental illness. Sleep and Mental Illness looks at this close correlation and considers the implications of research findings that have emerged in the last few years. Additionally, it surveys the essential concepts and practical tools required to deal with sleep and co-morbid psychiatric problems. The volume is divided into three main sections: basic science, neuroendocrinology, and clinical science. Included are over 30 chapters on topics such as neuropharmacology, insomnia, depression, dementia, autism, and schizophrenia. Relevant questionnaires for the assessment of sleep disorders, including quality-of-life measurement tools, are provided. There is also a summary table of drugs for treating sleep disorders. This interdisciplinary text will be of interest to clinicians working in psychiatry, behavioral sleep medicine, neurology, pulmonary and critical care medicine. © Cambridge University Press 2010.

Bahammam A.,King Saud University | Pandi-Perumal S.,Strategic Technologies Program | Pandi-Perumal S.,Somnogen Inc. | Alzoghaibi M.,King Saud University
Annals of Thoracic Medicine | Year: 2016

Aims: We hypothesized that if we control for lifestyle changes during Ramadan, Ramadan Islamic intermittent fasting (IF) reduces oxidative stress. This study was conducted to examine the effect of Islamic IF during and outside of Ramadan on the circadian changes in lipid peroxidation marker malondialdehyde (MDA) during and outside while controlling for potential confounders. Methods: Serum MDA concentration was measured in eight healthy male volunteers at baseline (BL), after fasting for 1 week before Ramadan (BL fasting), and during Ramadan. Blood samples were drawn at 22:00, 02:00, 04:00, 06:00, and 11:00. The participants were admitted to the sleep laboratory and monitored for 24 h on the day of the measurements. In the laboratory, each participant received meals of fixed compositions and caloric contents based on their ideal body weights. Light exposure, physical activity, and total sleep duration were uniformly maintained during the three study periods. Results: The participants had a mean age of 26.6 ± 4.9 years and a mean body mass index of 23.7 ± 3.5 kg/m2. No significant changes were observed in MDA levels and blood glucose during BL, BL fasting, or Ramadan. Conclusion: In this pilot study, under conditions of fixed sleep-wake schedules and caloric intake, Ramadan IF does not alter serum MDA levels in healthy subjects. Larger studies are needed to confirm these findings. © 2016 Annals of Thoracic Medicine.

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