A review of oxidative stress in acute kidney injury: protective role of medicinal plants-derived antioxidants

Palipoch, Sarawoot

doi:10.4314/ajtcam.v10i4.15

Cited by 44 publications

(41 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, ROS could induce lipid peroxidation (LPO) and result in a large production of secondary products, such as malondialdehye and 4-hydroxynonenal [46]. Those lipid peroxides could sustain free radical cascades and eventually lead to increased membrane rigidity as well as abnormal endothelial function, which may be involved in the pathophysiology of AKI [47][48][49].…”

Section: The Direct Antioxidant Function Of Vitamin E Though Inhibitimentioning

confidence: 99%

Protective effect of vitamin E against acute kidney injury

Liu

Feng

Wang

et al. 2015

BME

View full text Add to dashboard Cite

Abstract. It has been well-known for many years now that vitamin E is an essential nutrient; however, some of the physiological functions of this vitamin are still far from being understood. In recent years, a series of preclinical and clinical studies proposed a protective role of vitamin E on acute kidney injury (AKI), which has a high morbidity rate and mortality rate in clinical investigations. Based on the benefits associated with vitamin E, such as strong antioxidant function, low toxicity, rare side-effects, and low cost, this therapy strategy has garnered an extensive amount of interest in the scientific community for the development of new therapy modes against AKI. In this review, a concise overview of the application of vitamin E in the treatment of AKI is provided as well as a summary of a series of published data regarding the combination therapy modes and detailed therapy mechanisms of vitamin E-based therapy against AKI. At present, there are critical points of this therapy mode that are still in need of further clarification, meaning the current understanding of the role of vitamin E in the treatment of AKI remains incomplete. However, the development of more reliable pharmacological or biotechnical strategies with vitamin E for the eventual treatment of patients with AKI may guide the next chapter of vitamin E research.

show abstract

Section: The Direct Antioxidant Function Of Vitamin E Though Inhibitimentioning

confidence: 99%

Protective effect of vitamin E against acute kidney injury

Liu

Feng

Wang

et al. 2015

BME

View full text Add to dashboard Cite

show abstract

“…protein, DNA and lipid). Production of lipid peroxidation (LPO) in OS-related AKI results in large production of secondary products such as malondialdehye (MDA) and 4-hydroxynonenal [19,20].…”

Section: Discussionmentioning

confidence: 99%

Histopathological Evaluation of Dose Dependent Sulfadiazine-Associated Nephrotoxicity and Alteration on Oxidative Stress in Chicken Embryos

Sayrafi

Golshahi

Araghi

et al. 2016

Zahedan J Res Med Sci

View full text Add to dashboard Cite

Background: Numerous epidemiological and experimental researches indicate that in utero exposure to some environmental chemicals and prescribed drugs during pregnancy can mediate various embryonic abnormalities and complications via reactive oxygen species (ROS) generation, which damages cellular macromolecules. Objectives: The aim of the present study was to evaluate the sulfonamide-associated nephrotoxicity with possible underlying mechanisms in chicken embryo. Materials and Methods:In this experimental study, one hundred fertile eggs were obtained and divided into five groups: 1) control group (without injection), 2) group injected with 2 mg sulfadiazine, 3) group injected with 10 mg sulfadiazine, 4) group injected with 30 mg sulfadiazine and 5) group injected with 70 mg sulfadiazine. After hatching, the renal tissue from the newly hatched chick was harvested for histopathologic investigation and also measurement of oxidative stress parameters [the ferric reducing capacity assay, the glutathione content (GSH) and the situation of lipid peroxidation (LPO)] by spectrophotometer. Results: Histologic examination of the renal tissue revealed that sulfadiazine induces hydropic degeneration, tubular necrosis, glomerular and tubular atrophy, formation of hyaline cast, congestion, hemorrhage, interstitial nephritis and fibrosis. Conclusions: Result showed the dose-dependent administration of sulfadiazine significantly altered the histopathologic structure of renal tissues of chickens. Furthermore, the major histopathologic events in the course of sulfadiazine cytotoxicity are renal tubule epithelial cell necrosis, interstitial nephritis and fibrosis, formation of hyaline cast and congestion and hemorrhage, although sulfadiazine at dose 30 mg and 70 mg caused perturbation in antioxidant defense system by marked increase in LPO, and decrease in GSH.

show abstract

“…•-), hydroxyl radical ( •-through nicotinamide adenine dinucleotide phosphate oxidase (NOX) [5]. NOX1 and NOX4 are expressed in liver; NOX1 mainly produces O 2…”

Section: Ros Mainly Comprise Superoxide Radical (Omentioning

confidence: 99%