Vitamin D3 treatment regulates apoptosis, antioxidant defense system, and DNA integrity in the epididymal sperm of an aged rat model

Jeremy, Malsawmhriatzuala; Gurusubramanian, Guruswami; Roy, Vikas Kumar

doi:10.1002/mrd.23280

Cited by 8 publications

(4 citation statements)

References 67 publications

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“…As well, here, our results showed that d ‐gal increased MDA levels and decreased SOD and GPx activity in the heart and brain. Concerning vitamin D, Jeremy et al ( 2019 ) showed that it can delay testicular aging through the decrease in oxidative stress and the improvement of cellular antioxidant defense. In agreement, the present work shows that the two regimens of a low dose of vitamin D could decrease MDA levels and increase SOD and GPx activity, thus preventing and counteracting d ‐gal‐induced effects.…”

Section: Discussionmentioning

confidence: 99%

Distinct signatures on d‐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 SIRT1 and calstabin2 downregulation

Salemi,

Zamanian,

Giménez‐Llort

et al. 2023

Food Science & Nutrition

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Chronic administration of d‐galactose (d‐gal) in rodents reproduces the overproduction of reactive oxygen species of physiological aging. The present research shows for the first time distinct signatures on d‐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). d‐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 d‐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 d‐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.

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Section: Discussionmentioning

confidence: 99%

Distinct signatures on d‐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 SIRT1 and calstabin2 downregulation

Salemi,

Zamanian,

Giménez‐Llort

et al. 2023

Food Science & Nutrition

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“…The protective effect of 1α,25(OH) 2 D 3 on reproductive health has been elucidated 42 . Jeremy et al reported that 1α,25(OH) 2 D 3 can significantly improve the decline of male reproductive system function in aging rats through anti‐oxidation, reducing apoptosis, improving DNA integrity and spermatogenesis 43,44 . In addition, in diabetic rats, 1α,25(OH) 2 D 3 showed a certain protective effect on testicular function through suppressing inflammation and inhibiting cell apoptosis 45 .…”

Section: Discussionmentioning

confidence: 99%

1α,25‐dihydroxyvitamin D₃ supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response

Liang

et al. 2022

Environmental Toxicology

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Perfluorooctanesulfonate acid (PFOS) is a typical persistent organic pollutant that widely exists in the environment. To clarify the toxic effects and mechanisms of PFOS and to find effective intervention strategies have been attracted global attention. Here, we investigated the effects of PFOS on the male reproductive system and explored the potential protective role of 1α,25-dihydroxyvitamin D 3 (1α,25(OH) 2 D 3 ).Our results showed that 1α,25(OH) 2 D 3 intervention significantly improved PFOSinduced sperm quality decline and testicular damage. Moreover, 1α,25(OH) 2 D 3 aggrandized the total antioxidant capacity. Furthermore, after PFOS exposure, the transcription factor nuclear factor erythroid-related factor 2 (Nrf2) was adaptively increased together with its target genes, such as HO-1, NQO1, and SOD2. Meanwhile, 1α,25(OH) 2 D 3 ameliorated PFOS-induced augment of Nrf2 and target genes.These findings indicated that 1α,25(OH) 2 D 3 might attenuate PFOS-induced reproductive injury in male mice via Nrf2-mediated oxidative stress. K E Y W O R D S 1α,25(OH) 2 D 3 , Nrf2, oxidative stress, perfluorooctanesulfonate acid, reproductive toxicity 1 | INTRODUCTION Perfluorooctanesulfonic acid (PFOS) is a representative synthetic organo-fluorine compound, which has been widely used as a stain repellent and anti-stick material due to its excellent hydrophobic and lipophobic properties. 1 However, PFOS is difficult to degrade and widely exists in water, dust, soil, and other environmental media. 2,3 Noteworthy, PFOS generates a bioaccumulation effect. Drinking water, contaminated food consumption, product usage, and occupational exposure are the main approaches to PFOS exposure. PFOS has been extensively detected in human blood, umbilical cord blood, breast milk, and other samples worldwide. 4 Therefore, PFOS exposure has become a global environmental problem, and it is of great importance to clarify the toxic effects and mechanisms of PFOS and to find effective intervention strategies.In human body, PFOS combines with proteins, such as liver fatty acid transporters in the liver and albumin in the plasma. Liver is the primary target of PFOS, which can cause typical hepatic toxicity by disrupting glucose and lipid metabolism. [5][6][7][8] Recent studies have discovered that PFOS can also induce immune toxicity, 9 cardiotoxicity, 10 and neurotoxicity. 11 Furthermore, PFOS has significant reproductive

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“…VD induces an overall pro-survival transcriptional program characterized by upregulated expression of anti-apoptotic genes and downregulated expression of pro-apoptotic genes [ 142 ]; in addition, VD determines the non-genomic activation of the PI3K-Akt survival kinase pathway [ 143 ], it also reduces apoptosis of EC by increasing NO production (see above) .…”

Section: Vitamin D In Diabetic Retinopathymentioning

confidence: 99%

Role of vitamin D in diabetic retinopathy: Pathophysiological and clinical aspects

Tecilazich

Formenti

Giustina

2020

Rev Endocr Metab Disord

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Epidemiological data predict a dramatic increase in the prevalence of diabetes and of diabetic retinopathy (DR)the most common complication of diabetes-for which however we do not have so far effective tools for prevention and treatment. Since hypovitaminosis D is very frequent in patients with diabetes and vitamin D (VD) has vascular protective properties, several studies have addressed the association of VD deficiency with DR and its severity and progression, whereas the effects of VD supplementation on its natural history are largely unknown. Here we review the available evidence that supports the possible protective role of VD in DR and suggests to determine the VD levels in DR patients calling for a definitive randomized clinical trial to ascertain whether VD supplementation could protect against DR.

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Vitamin D3 treatment regulates apoptosis, antioxidant defense system, and DNA integrity in the epididymal sperm of an aged rat model

Cited by 8 publications

References 67 publications

Distinct signatures on d‐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 SIRT1 and calstabin2 downregulation

Distinct signatures on d‐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 SIRT1 and calstabin2 downregulation

1α,25‐dihydroxyvitamin D₃ supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response

Role of vitamin D in diabetic retinopathy: Pathophysiological and clinical aspects

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Vitamin D3 treatment regulates apoptosis, antioxidant defense system, and DNA integrity in the epididymal sperm of an aged rat model

Cited by 8 publications

References 67 publications

Distinct signatures on d‐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 SIRT1 and calstabin2 downregulation

Distinct signatures on d‐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 SIRT1 and calstabin2 downregulation

1α,25‐dihydroxyvitamin D3 supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response

Role of vitamin D in diabetic retinopathy: Pathophysiological and clinical aspects

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1α,25‐dihydroxyvitamin D₃ supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response