title: Melatonin reduces oxidative stress in erythrocytes and plasma of senescence-accelerated mice.
abstract: It has been suggested that oxidative stress is a feature of aging. The goal of the present study was to assess the oxidant effects related to aging and the protective role of exogenous melatonin in senescence-accelerated mice (SAMP8). Two groups of SAMP8 mice (males and females) were compared with their respective control groups of SAMR1 mice (senescence-resistant inbred strain) to determine their oxidative status without melatonin treatment. Four other groups of the same characteristics were treated with melatonin (10 mg/kg/day) in their drinking water. The melatonin concentration in the feeding bottles was titrated according to water consumption and body weight (i.e. 0.06 mg/mL for 30 g of body weight and 5 mL/day of water consumption). The treatment began when animals were 1-month old and continued for 9 months. When mice were 10-month old, they were anesthetized and blood was obtained. Plasma and erythrocytes were processed to examine oxidative stress markers: reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), thiobarbituric acid reactive substances (TBARS), and hemolysis. The results showed greater oxidative stress in SAMP8 than in SAMR1, largely because of a decrease in GSH levels and to an increase in GSSG and TBARS with the subsequent induction of the antioxidant enzymes GPX and GR. Melatonin, as an antioxidant molecule, improved the glutathione-related parameters, prevented the induction of GPX in senescent groups, and promoted a decrease in SOD and TBARS in almost all the groups.
authors.affiliation: Unit of Pharmacology, School of Medicine and Health Sciences, Rovira i Virgili University, Reus, Spain. mariarosa.nogues@urv.net
authors.forename: M Rosa
authors.initials: MR
authors.lastname: Nogués
authors.forename: Montserrat
authors.initials: M
authors.lastname: Giralt
authors.forename: Marta
authors.initials: M
authors.lastname: Romeu
authors.forename: Miquel
authors.initials: M
authors.lastname: Mulero
authors.forename: Vanesa
authors.initials: V
authors.lastname: Sánchez-Martos
authors.forename: Esperanza
authors.initials: E
authors.lastname: Rodríguez
authors.forename: Darío
authors.initials: D
authors.lastname: Acuña-Castroviejo
authors.forename: Jordi
authors.initials: J
authors.lastname: Mallol
mesh_terms: D000375:Aging; D019588:Aging, Premature; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D004912:Erythrocytes / Q000737:chemistry* / Q000201:enzymology; D005260:Female; D005978:Glutathione / Q000097:blood / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008297:Male; D008550:Melatonin / Q000008:administration & dosage / Q000494:pharmacology*; D051379:Mice; D008815:Mice, Inbred Strains; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D013858:Thiobarbiturates / Q000097:blood / Q000378:metabolism
chemical_list: D000975:Antioxidants; D013858:Thiobarbiturates; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D008550:Melatonin; C029684:thiobarbituric acid