Vitamin D attenuates gentamicin-induced acute renal damage via prevention of oxidative stress and DNA damage

Abstract

<jats:sec><jats:title>Background:</jats:title><jats:p> Despite being one of the most nephrotoxic drugs, gentamicin (GM) remains a mainstay as a first-choice agent in a vast variety of clinical situations owing to its superlative efficiency as a broad-spectrum antibiotic in treating several life-threatening bacterial infections. This urgently calls for the need for in-depth analysis of the mechanisms governing GM-induced nephrotoxicity and entails the necessity of presenting novel protective agents capable of ameliorating those renal deleterious effects. The reactive oxygen species and redox-sensitive transcription factors in GM-induced nephrotoxicity have recently called attention. </jats:p></jats:sec><jats:sec><jats:title>Purpose:</jats:title><jats:p> This study has been designed to shed light on the possible mechanisms of GM-induced nephrotoxicity and to provide a consensus set of histopathological, immunohistochemical, genetic and biochemical parameters elucidating the protective role of vitamin D against this nephrotoxicity. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> Twenty-four adult male albino rats were equally divided into four groups: group I (control group), group II (GM), group III (GM + vitamin D) and group IV (vitamin D only). Kidney function tests, histopathological examination, gene expression of nuclear factor 2, nuclear factor kappa beta (NF-κB) and western blot of NF-κB p65, assessment of glutathione peroxidase and nicotinamide adenine dinucleotide phosphate oxidase (NADPH) oxidase by ELISA, as well as immunohistochemical evaluation of inducible nitric oxide, malondialdehyde, 8-hydroxy 2 deoxyguanine and vitamin D receptor, have been carried out. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> The kidney function deterioration, tissue oxidative stress development and the histopathological changes induced by GM were significantly attenuated by vitamin D administration. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> Vitamin D attenuates GM nephrotoxicity through its antioxidant properties and prevention of DNA damage. </jats:p></jats:sec>

Evaluation of the protective effect of paricalcitol and vitamin D3at doxorubicin nephrotoxicity in rats with99mTechnetium-dimercaptosuccinic acid renal scintigraphy and biochemical methods

“…A number of studies confirmed the crucial role of vit D 3 as a potent antioxidant. 59 –61 Additionally, many studies have displayed the role of vit D 3 in the regulation of inducible form of NOS. 62,63 Garcion et al 62 mentioned that vit D 3 exerts its protecting effects through preventing free radical formation by the reactive species of nitric oxide and oxygen.…”

A novel protective role of sacubitril/valsartan in cyclophosphamide induced lung injury in rats: impact of miRNA-150-3p on NF-κB/MAPK signaling trajectories

“…The mRNA expression of β-actin was considered as the internal control, and all the assessment and analysis of all data was processes using the comparative cycle threshold (CT) method. The primers used for Nrf2 , NF-κB and β-actin were (Nrf2; Forward primer: 5′-GCT GCA GAA GCA AGA GAA CC-3′ and Reverse primer: 5′-GGCAGTGAAGACTGAACTTTCA-3′, GenBank accession number NM031789.2 58 , NF-κB; Forward primer: 5′-CATTGAGGTGTATTTCACGG-3′, Reverse primer :5′-GGCAAGTGGCCATTGTGTTC-3′, GenBank accession number NM199267.2) 59 , β-actin; Forward primer: 5′-GACGGCCAGGTCATCACTAT-3′, Reverse primer: 5′-CTTCTGCATCCTGTCAGCAA-3′, GenBank accession number XM011332812.3 ) 58 .…”

Vitamin D3attenuates cisplatin-induced intestinal injury by inhibiting ferroptosis, oxidative stress, and ROS-mediated excessive mitochondrial fission

“…14 Vitamin D 3 has anti-oxidative properties, reduces inflammatory response, and improves immunity. 15,16 Vitamin D 3 is also effective in inflammatory bowel disease, 17 pulmonary fibrosis, 18 and renal fibrosis. 19 However, little is known about the role of vitamin D 3 in CP-induced intestinal injury; in particular, the relationship between vitamin D 3 and intestinal oxidative stress and ferroptosis is not known.…”