Vitamin D3 deficiency increases DNA damage and the oxidative burst of neutrophils in a hypertensive rat model

Machado, Carla da Silva; Venâncio, Vinícius Paula; Aissa, Alexandre Ferro; Hernandes, Lívia Cristina; Mello, Michela Bianchi de; Lama, José Eduardo Cavalcanti Del; Marzocchi-Machado, Cleni Mara; Bianchi, Marcelo; Antunes, Lusânia Maria Greggi

doi:10.1016/j.mrgentox.2016.01.005

Cited by 23 publications

(20 citation statements)

References 57 publications

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“…This is an important finding as alterations in paternal chromatin can have dramatic consequences on reproduction especially if the oocyte is unable to repair such paternal nuclear damage. Given the extensive antioxidant and regulatory roles of vitamin D on gene expression, 60‐67 further studies are needed to determine which processes (either in the testis during spermatogenesis or in the epididymis during post‐testicular maturation) could be affected.…”

Section: Discussionmentioning

confidence: 99%

Impact of vitamin D deficiency on mouse sperm structure and function

et al. 2020

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Background In rodents and humans, vitamin D deficiency (VDD) is associated with altered sperm structure and function (primarily decreased motility and morphological abnormalities) that are primarily attributed to VDD‐induced hypocalcemia. However, it is suspected that VDD has much more drastic effects on mammalian spermatozoa. Objectives The purpose of this study was to illustrate that VDD, depending on its severity and duration, can alter sperm nuclear integrity and can also lead to the loss of spermatozoa's ability to support embryonic development. Materials and methods A mouse model of induced VDD combining the action of a vitamin D‐deficient diet, UV exposure limitation, and paricalcitol injections; a vitamin D2 analog that catabolizes endogenous vitamin D by increasing the expression of CYP24A, a member of the cytochrome P450 family, has been used to create different grades of VDD. Results We show that the most significant sperm defect recorded concerns the integrity of the paternal nucleus, which is both decondensed and fragmented in moderate‐to‐severe VDD situations. Consistent with the known consequences of fertilization with DNA‐damaged spermatozoa, we show that paternal VDD decreases the ability of spermatozoa to optimally support fertilization and embryonic development. Discussion and Conclusion Given the worldwide high prevalence of VDD in humans, and although obtained in an animal model, the data presented here suggest that subfertile/infertile males may benefit from VDD testing and that attempts to correct serum vitamin D levels could be considered prior to conception, either naturally or through ART.

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Section: Discussionmentioning

confidence: 99%

Impact of vitamin D deficiency on mouse sperm structure and function

et al. 2020

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“…The VD3 treatment was shown to increase cell viability and to decrease ROS production, in cone cells under oxidative stress [56]. Furthermore, VD3 deficiency induced ROS production by neutrophil, in spontaneous hypertensive rats [57], and prevented oxidative stress in adipose tissue of diabetic mice [58]. These data agree with ours, showing that VD3 treatments significantly decreased nitrite contents and lipoperoxidation in lesioned striata, as related to the same area of the non-treated 6-OHDA rats, indicating that VD3 presents an antioxidant action.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats

Lima

Lopes

Costa

et al. 2018

J Neuroinflammation

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BackgroundThe deficiency in 1α, 25-dihydroxyvitamin D3 (VD3) seems to increase the risk for neurodegenerative pathologies, including Parkinson’s disease (PD). The majority of its actions are mediated by the transcription factor, VD3 receptor (VD3R).MethodsThe neuroprotective effects of VD3 were investigated on a PD model. Male Wistar rats were divided into the following groups: sham-operated (SO), 6-OHDA-lesioned (non-treated), and 6-OHDA-lesioned and treated with VD3 (7 days before the lesion, pre-treatment or for 14 days after the 6-OHDA striatal lesion, post-treatment). Afterwards, the animals were subjected to behavioral tests and euthanized for striatal neurochemical and immunohistochemical assays. The data were analyzed by ANOVA and the Tukey test and considered significant for p < 0.05.ResultsWe showed that pre- or post-treatments with VD3 reversed behavioral changes and improved the decreased DA contents of the 6-OHDA group. In addition, VD3 reduced the oxidative stress, increased (TH and DAT), and reduced (TNF-alpha) immunostainings in the lesioned striata. While significant decreases in VD3R immunoreactivity were observed after the 6-OHDA lesion, these changes were blocked after VD3 pre- or post-treatments. We showed that VD3 offers neuroprotection, decreasing behavioral changes, DA depletion, and oxidative stress. In addition, it reverses partially or completely TH, DAT, TNF-alpha, and VD3R decreases of immunoreactivities in the non-treated 6-OHDA group.ConclusionsTaken together, VD3 effects could result from its anti-inflammatory and antioxidant actions and from its actions on VD3R. These findings should stimulate translational research towards the VD3 potential for prevention or treatment of neurodegenerative diseases, as PD.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1266-6) contains supplementary material, which is available to authorized users.

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“…Kidney samples were embedded in the optimum cutting temperature (OCT) formulation (Tissue-Tek, Torrance, CA, USA) after being fixed in 4 % paraformaldehyde for 24 h performed the comet assay as described by Tice et al (29) and Machado et al (30). Cell viability was above 90 %, according to the trypan blue dye exclusion method.…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

Nephrotoxicity and genotoxicity of silver nanoparticles in juvenile rats and possible mechanisms of action

Liu

Sun

Yang

et al. 2020

Archives of Industrial Hygiene and Toxicology

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AbstractBecause of their widespread use and potential adverse effects in young developing organism, this study focused on the nephrotoxicity and genotoxicity of chronic low-dose exposure to silver nanoparticles (AgNPs) in 32 14-day-old male Wistar rats, randomly divided into three groups receiving AgNP solution (3 mg/kg body weight) intraperitoneally for one, two, or three weeks and the untreated control group (eight animals per group). When the rats were eight weeks old, blood creatinine and urine microalbumin were tested, followed by haematoxylin and eosin (H&E) staining. Proteinuria was found in the animals treated with AgNP for three weeks, and H&E staining revealed pathological changes in the kidney sections of this group. DNA damage was detected with the alkaline comet assay in the groups treated for two and three weeks. All results indicate that chronic exposure, even at a low dose, may affect animal health. The main culprit might be increased and time-dependent reactive oxygen species (ROS) production. Highly reactive ROS could cause a major structural damage to proteins and DNA, change the expression of ion channel proteins, and trigger inflammation. The findings of our in vivo experiment raise concern about nephrotoxic and genotoxic effects of silver nanoparticles in young organisms and call for further investigation of nanoparticle properties that can be modified to minimise the risks.

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Vitamin D3 deficiency increases DNA damage and the oxidative burst of neutrophils in a hypertensive rat model

Cited by 23 publications

References 57 publications

Impact of vitamin D deficiency on mouse sperm structure and function

Impact of vitamin D deficiency on mouse sperm structure and function

Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats

Nephrotoxicity and genotoxicity of silver nanoparticles in juvenile rats and possible mechanisms of action

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