Evaluations of lipid peroxidation and inflammation in short‐term glycerol‐induced acute kidney injury in rats

Nara, Akina; Yajima, Daisuke; Abe, Hiroko; Hoshioka, Yumi; Iwase, Hirotaro

doi:10.1111/1440-1681.12633

Cited by 22 publications

(17 citation statements)

References 41 publications

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“…The mechanism of rhabdomyolysis‐induced AKI is proposed as follows: the skeletal muscle cell membrane is injured, Mb in skeletal muscle leaks into the blood, Mb accumulates in the kidney cells, and oxidative stress‐induced kidney injury caused via Mb redox cycling generates oxidized lipids. These oxidized lipids propagate renal tissue injury (Boutaud & Roberts, ; Nara et al, ). Thus, Mb leaked from skeletal muscle is known to be a key mediator for AKI.…”

Section: Discussionmentioning

confidence: 99%

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Acute kidney injury model established by systemic glutathione depletion in mice

Matsubara

Oda

Jia

et al. 2019

J of Applied Toxicology

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Glutathione (GSH) is one of the most extensively studied tripeptides. The roles for GSH in redox signaling, detoxification of xenobiotics and antioxidant defense have been investigated. A drug‐induced rhabdomyolysis mouse model was recently established in L‐buthionine‐(S,R)‐sulfoximine (BSO; a GSH synthesis inhibitor)‐treated normal mice by co‐administration of antibacterial drug and statin. In these models, mild kidney injury was observed in the BSO only‐treated mice. Therefore, in this study, we studied kidney injury in the GSH‐depleted mouse. BSO was intraperitoneally administered twice a day for 7 days to normal mice. The maximum level of plasma creatine phosphokinase (351 487 ± 53 815 U/L) was shown on day 8, and that of aspartate aminotransferase was shown on day 6. Increased levels of blood urea nitrogen, plasma creatinine, urinary kidney injury molecule‐1 and urinary creatinine were observed. An increase of mRNA expression level of renal lipocalin 2/neutrophil gelatinase‐associated lipocalin was observed. Degeneration and necrosis in the skeletal muscle and high concentrations of myoglobin (Mb) in blood (347‐203 925 ng/mL) and urine (2.5‐68 583 ng/mL) with large interindividual variability were shown from day 5 of BSO administration. Mb‐stained regions in the renal tubule and renal cast were histologically observed. In this study, the GSH‐depletion treatment established an acute kidney injury mouse model due to Mb release from the damaged skeletal muscle. This mouse model would be useful for predicting potential acute kidney injury risks in non‐clinical drug development.

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Section: Discussionmentioning

confidence: 99%

“…BSO, Lbuthionine-(S,R)-sulfoximine; GSH, glutathione; GSSG, glutathione disulfide generates oxidized lipids. These oxidized lipids propagate renal tissue injury (Boutaud & Roberts, 2011;Nara et al, 2016). Thus, Mb leaked from skeletal muscle is known to be a key mediator for AKI.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury model established by systemic glutathione depletion in mice

Matsubara

Oda

Jia

et al. 2019

J of Applied Toxicology

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“…Oxidative injury mediated by lipid peroxidation is an unfavorable factor for AKI [ 85 ], while lipid peroxidation inhibition can alleviate kidney injury [ 86 ]. One month before Dixon proposed ferroptosis, some researchers found that deferoxamine (DFO), which was not listed as a ferroptosis inhibitor then, could inhibit lipid peroxidation and renal tubular epithelial cell necrosis to prevent renal failure [ 87 ].…”

Section: Ferroptosis and Akimentioning

confidence: 99%

The Cross‐Link between Ferroptosis and Kidney Diseases

Wang

Liu

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Acute and chronic kidney injuries result from structural dysfunction and metabolic disorders of the kidney in various etiologies, which significantly affect human survival and social wealth. Nephropathies are often accompanied by various forms of cell death and complex microenvironments. In recent decades, the study of kidney diseases and the traditional forms of cell death have improved. Nontraditional forms of cell death, represented by ferroptosis and necroptosis, have been discovered in the field of kidney diseases, which have reshuffled the role of traditional cell death in nephropathies. Although interactions between ferroptosis and acute kidney injury (AKI) have been continuously explored, studies on ferroptosis and chronic kidney disease (CKD) remain limited. Here, we have reviewed the therapeutic significance of ferroptosis in AKI and anticipated the curative potential of ferroptosis for CKD in the hope of providing insights into ferroptosis and CKD.

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“…However, that adaptation resulted in some technical variations, both in the storage media used (10% or 15% glycerol, or D5W alone) and in the strategy of filtration to remove particulate (multistage filtration through a 860 µm and, then, a 190 µm filter, or individual filtrations through 100 µm or 70 µm filters) 13,14,15 . The injection of glycerol alone could potentially cause harm, given that 25%-50% glycerol injections have been used as a rodent model of renal injury 16,17,18,19,20 . To avoid unintended side effects of glycerol, the cecal slurry stock preparation for mice in this study is frozen in D5W without glycerol, and tests of bacterial viability from storage at -80 °C are performed.…”

Section: Introductionmentioning

confidence: 99%

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis

Brook

Amenyogbe

Ben‐Othman

et al. 2019

JoVE

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Neonatal sepsis remains a global burden. A preclinical model to screen effective prophylactic or therapeutic interventions is needed. Neonatal mouse polymicrobial sepsis can be induced by injecting cecal slurry intraperitoneally into day of life 7 mice and monitoring them for the following week. Presented here are the detailed steps necessary for the implementation of this neonatal sepsis model. This includes making a homogeneous cecal slurry stock, diluting it to a weight-and litter-adjusted dose, an outline of the monitoring schedule, and a definition of observed health categories used to define humane endpoints. The generation of a homogeneous cecal slurry stock from pooled donors allows for the administration into many litters over time, reducing the variation between donors, and preventing the use of potentially toxic glycerol. The monitoring strategy used allows for the anticipation of survival outcome and the identification of mice that would later progress to death, allowing for an earlier identification of the humane endpoint. Two main behavioral features are used to define the health scores, namely, the ability of the neonatal mice to right themselves when placed on their back and their level of mobility. These criteria could potentially be applied to address humane endpoints in other studies of neonatal disease in mice, as long as a pilot study is performed to confirm accuracy. In conclusion, this approach provides a standardized method to model newborn sepsis in mice, while providing resources to assess animal welfare used to define early humane endpoints for challenged animals.

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Evaluations of lipid peroxidation and inflammation in short‐term glycerol‐induced acute kidney injury in rats

Cited by 22 publications

References 41 publications

Acute kidney injury model established by systemic glutathione depletion in mice

Acute kidney injury model established by systemic glutathione depletion in mice

The Cross‐Link between Ferroptosis and Kidney Diseases

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis

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