Distinct signatures on <scp>d</scp>‐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 <scp>SIRT1</scp> and calstabin2 downregulation

Chronic administration of d-galactose (d-gal) in rodents reproduces the overproduction reactive oxygen species physiological aging. The present research shows for first time distinct signatures on d-gal-induced aging (500 mg/kg, 6 weeks) and preventive protective potential two vitamin D (50 IU) supplementation regimens (pre-induction simultaneous, respectively) vital organs (heart brain). notorious alterations working memory, a strong increase brain malondialdehyde (MDA) oxidative levels, downregulation sirtuin 1 (SIRT1) heart hippocampus calstabin2 heart. Cardiac superoxide dismutase (SOD) glutathione peroxidase (GPx) enzymatic antioxidant capacities were damaged, was downregulated, neuropathology observed. Heart damage also included moderate MDA serologic lactate dehydrogenase (LDH), total creatine kinase (CK) activities, histopathological alterations. used dose enough to prevent cognitive impairment, avoid muscular damage, hamper cardiac cerebral stress, SIRT1 downregulation. Most importantly, potencies schedules depended tissue level study. pre-induction schedule prevented by order magnitude higher than simultaneous all variables studied except SIRT1, whose induced d-gal equally both schedules. benefits stress stronger Brain levels more sensitive while SOD GPx activities In this order, SOD, MDA, markers prevention. summary, results unveiled induction, signatures, sensitivity depending different study tissues, which are relevant from mechanistic view design targeted interventions.