Ischemia/reperfusion (I/R) is one of the major causes of acute kidney injury (AKI) and associated with increased mortality and progression to chronic kidney injury (CKI). Molecular mechanisms underlying I/R injury involve the production and excessive accumulation of reactive oxygen species (ROS). Peroxiredoxin (Prx) V, a cysteine-dependent peroxidase, is located in the cytosol, mitochondria, and peroxisome and has an intensive ROS scavenging activity. Therefore, we focused on the role of Prx V during I/R-induced AKI using Prx V knockout (KO) mice. Ablation of Prx V augmented tubular damage, apoptosis, and declined renal function. Prx V deletion also showed higher susceptibility to I/R injury with increased markers for oxidative stress, ER stress, and inflammation in the kidney. Overall, these results demonstrate that Prx V protects the kidneys against I/R-induced injury.
Abstract. This research was conducted to evaluate the influence of NO 3 -:NH 4 + ratios in fertilizer solution on the vegetative growth and fruit yield of hot pepper (Capsicum annuum L.) through pot cultivation. The Hoaglad's solution was modified to contain various NO 3 -:NH 4 + ratios such as 100:0 (A), 73:37 (B), 50:50 (C), 27:73 (D), 0:100 (E), and no nitrogen (F). Plants were transplanted into root substrates and the modified solutions were applied as plant needed in plastic house. There were no statistical significances among the treatments from A through D in the fresh and dry weights, and number of leaves 31 days after transplanting, but elevation of NH 4 + ratios in the solution decreased the fresh fruit weight 62 days after transplanting with statistical differences. In the results of inorganic element analysis based on the dry weight of fully expanded mature leaves, N and P contents as well as micro cations such as Fe, Mn, Zn, and Cu increased as NH 4 + ratios were elevated 62 days after transplanting. However, those of macro cations such as K, Ca, and Mg resulted in decreasing tendency. The elevation of NH 4 + ratios in fertilizer solution resulted in the increase of EC and total N concentrations (NO 3 -+ NH 4 + ), but this decreased the pH as well as Ca and Mg concentrations in soil solution 62 days after transplanting. The K concentration in soil solution was the highest in the treatments of C and followed by D, B, E, and A. The above results indicate that the proper NO 3 -:NH 4 + ratio in the nutrient solution is 73:27 (B) or 100:0 (A) and the B solution is proper for the vegetative growth and that of A is proper for reproductive growth stage.
Non-alcoholic fatty liver disease (NAFLD) is emerging as the most common chronic liver disease worldwide. In addition, NAFLD may increase the risk of cardiovascular and liver-related diseases, and displays features of metabolic syndrome. In NAFLD, oxidative stress is primarily caused by excessive free fatty acids. The oxidation of fatty acids is usually caused by β-oxidation of mitochondria under normal conditions, resulting in the production of energy. However, when the inflow of fatty acids in NAFLD becomes excessive, the β-oxidation of mitochondria becomes saturated and the oxidation process increases at sites including peroxisomes and microsomes, thereby increasing production of reactive oxygen species (ROS). Thus, hepatic mitochondrial ROS play an important role in the pathogenesis of NAFLD. Eliminating mitochondrial ROS may improve NAFLD, but the underlying mechanism remains unclear. We examined the effect of mitochondrial ROS on NAFLD by focusing on peroxiredoxin (Prx), an antioxidant protein that can remove hydrogen peroxide. The protective effect and pathological phenomenon of mitochondrial peroxiredoxin in methionine-choline deficient diet (MCD)-induced liver injury was assessed in a mouse model of NAFLD. In these mice, mitochondrial peroxiredoxin deficiency significantly increased hepatic steatosis and fibrosis. In addition, ablation of Prx III enhances susceptibility to MCD diet-induced oxidative stress and exacerbates NAFLD progression by promoting inflammation. The binding assay results also showed that Prx III-deficient mice had more severe liver damage than Prx III-abundant mice in MCD diet liver injury models. The present data suggest that mitochondrial peroxiredoxin III could be a therapeutic target for preventing and suppressing diet-induced NAFLD.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
334 Leonard St
Brooklyn, NY 11211
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.