title: Late-onset dietary restriction compensates for age-related increase in oxidative stress and alterations of HSP 70 and synapsin 1 protein levels in male Wistar rats.
abstract: Numerous reports implicate increased oxidative stress in the functional and structural changes occurring in the brain and other organs as a part of the normal aging process. Dietary restriction (DR) has long been shown to be life-prolonging intervention in several species. This study was aimed to assess the potential efficacy of late-onset short term DR when initiated in 21 months old male wistar rats for 3 months on the antioxidant defense system and lipid peroxidation, cellular stress response protein HSP 70 and synaptic marker protein synapsin 1 in discrete brain regions such as cortex, hypothalamus, and hippocampus as well as liver, kidney and heart from 24 month old rats. Age-associated decline in activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione, and elevated levels of lipid peroxidation was observed in brain and peripheral organ as well as increased expression of HSP 70 and reduction in synapsin 1 was observed in brain studied. Late-onset short term DR was effective in partially restoring the antioxidant status and in decreasing lipid peroxidation level as well as enhancing the expression of HSP 70 and synapsin 1 in aged rats. Late onset short term DR also prevented age-related neurodegeneration as revealed by Fluoro-Jade B staining in hippocampus and cortex regions of rat brain. Thus our current results suggest that DR initiated even in old age has the potential to improve age related decline in body functions.
authors.affiliation: Department of Biotechnology, Guru Nanak Dev University, Amritsar, Punjab, India.
authors.forename: Sandeep
authors.initials: S
authors.lastname: Sharma
authors.forename: Rumani
authors.initials: R
authors.lastname: Singh
authors.forename: Manpreet
authors.initials: M
authors.lastname: Kaur
authors.forename: Gurcharan
authors.initials: G
authors.lastname: Kaur
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D004038:Diet, Reducing; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology; D008099:Liver / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D016704:Synapsins / Q000378:metabolism*
chemical_list: D018840:HSP70 Heat-Shock Proteins; D016704:Synapsins; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione