Distinct signatures on -galactose-induced aging and preventive/protective potency of two low-dose vitamin D supplementation regimens on working memory, muscular damage, cardiac and cerebral oxidative stress, and and calstabin2 downregulation
Salemi, Sahar (Rafsanjan University of Medical Sciences (Iràn))
Zamanian, Mohammad Yasin (Hamadan University of Medical Sciences (Iràn))
Gimenez-Llort, Lydia (Universitat Autònoma de Barcelona. Departament de Psiquiatria i de Medicina Legal)
Jalali, Zahra (Rafsanjan University of Medical Sciences (Iràn))
Mahmoodi, Mehdi (Kerman University of Medical Sciences (Iràn))
Golmohammadi, Maryam (Shahid Beheshti University of Medical Sciences (Iràn))
Kaeidi, Ayat (Rafsanjan University of Medical Sciences (Iràn))
Taghipour, Zahra (Rafsanjan University of Medical Sciences (Iràn))
Khademalhosseini, Morteza (Rafsanjan University of Medical Sciences (Iràn))
Modanloo, Mona (Mazandaran University of Medical Sciences (Iràn))
Hajizadehi, Mohammad Reza (Rafsanjan University of Medical Sciences (Iràn))

Data:	2023
Resum:	Chronic administration of -galactose (-gal) in rodents reproduces the overproduction of reactive oxygen species of physiological aging. The present research shows for the first time distinct signatures on -gal-induced aging (500 mg/kg, 6 weeks) and the preventive and protective potential of two vitamin D (50 IU) supplementation regimens (pre-induction and simultaneous, respectively) in two vital organs (heart and brain). -gal-induced notorious alterations in working memory, a strong increase in brain malondialdehyde (MDA) oxidative levels, and strong downregulation of sirtuin 1 (SIRT1) in the heart and hippocampus and of calstabin2 in the heart. Cardiac and brain superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymatic antioxidant capacities were damaged, brain calstabin2 was downregulated, and neuropathology was observed. Heart damage also included a moderate increase in MDA levels, serologic lactate dehydrogenase (LDH), total creatine kinase (CK) activities, and histopathological alterations. The used dose of vitamin D was enough to prevent cognitive impairment, avoid muscular damage, hamper cardiac and cerebral oxidative stress, and SIRT1 and calstabin2 downregulation. Most importantly, the potencies of the two preventive schedules depended on the tissue and level of study. The pre-induction schedule prevented -gal-induced aging by 1 order of magnitude higher than simultaneous administration in all the variables studied except for SIRT1, whose strong downregulation induced by -gal was equally prevented by both schedules. The benefits of vitamin D for oxidative stress were stronger in the brain than in the heart. Brain MDA levels were more sensitive to damage, while SOD and GPx antioxidant enzymatic activities were in the heart. In this order, the magnitude of SOD, MDA, and GPx oxidative stress markers was sensitive to prevention. In summary, the results unveiled distinct aging induction, preventive signatures, and sensitivity of markers depending on different levels of study and tissues, which are relevant from a mechanistic view and in the design of targeted interventions. Heart and brain -gal-induced aging and preventive potencies of two Vit D regimes were distinct. -gal-induced impairment was notorious in cognition and brain MDA levels and prevented by Vit D.
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Matèria:	Aging ; Calstabin2 ; Oxidative stress ; SIRT1 ; Vitamin D
Publicat a:	Food Science & Nutrition, Vol. 11 (may 2023) , p. 5050-5062, ISSN 2048-7177

DOI: 10.1002/fsn3.3422
PMID: 37701236

13 p, 3.1 MB

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