Oxidative stress mediates renal endothelial cell damage in trichloroethylene-sensitized mice

Abstract

The purpose of this study was to explore whether renal endothelial cell injury is associated with oxidative stress in trichloroethylene (TCE)-induced immune kidney damage by detecting adhesion molecules and oxidative stress indexes. In this study, a mouse model of skin sensitization with the antioxidant Tempol was used to explore the mechanism. Blood urea nitrogen (BUN), creatinine (Cre), and histological examination were used for kidney function evaluation. Kidney homogenates were used for detecting renal nitric oxide (NO), nitric oxide synthase (NOS), superoxide dismutase (SOD) and malondialdehyde (MDA). Renal endothelial nitric oxide synthase (eNOS), E-selectin, vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecule (ICAM-1) protein levels were measured by immunohistochemical and Western blot. We found that BUN and Cre levels increased in the TCE sensitization positive group and the TCE+Tempol sensitization positive group. In the TCE sensitization positive group, a partial area of vacuolar degeneration and lysed epithelial cells were observed in renal tubules. In TCE+Tempol sensitization positive group, small areas were also found to be vacuolar degenerated and renal tubules were dissolved. Renal NO, NOS, SOD and eNOS levels decreased and MDA levels increased, renal E-selectin, VCAM-1and ICAM-1 protein levels increased in the TCE sensitization positive group and the TCE+Tempol sensitization positive group. Tempol attenuated TCE induced up-regulation of MDA, E-selectin, VCAM-1and ICAM-1 and downregulation of NO, NOS, SOD and eNOS. In conclusion, trichloroethylene-sensitized mice renal immune injury is associated with the renal endothelial cells' oxidative stress state.

Beneficial effects of procyanidin B2 on adriamycin-induced nephrotic syndrome mice: the multi-action mechanism for ameliorating glomerular permselectivity injury

“…80,81 Meanwhile, owing to the abundance of PUFAs, endothelial cells are susceptible to ROS damage. 82 Thus, the harmful levels of ROS lead to cellular lipid membrane peroxidation; this also agrees with previous studies showing that MDA production is significantly elevated in oxidative stress due to ROS and PUFAs. 83 Increased activation of renal ROS, PUFAs, and MDAs in this study supports these earlier findings.…”

Predictors of Renal Function Worsening in Patients with Chronic Obstructive Pulmonary Disease (COPD): A Multicenter Observational Study

“…Moreover, cigarette smoking exerts an indirect pathogenic action by injuring pulmonary vascular endothelium. A similar endothelial damage can be also induced in mouse models at the level of renal vessels [ 51 ]. Oxidative stress also leads to an enlarged synthesis of advanced glycation end products (AGEs), which in turn activate their receptors (RAGEs) [ 52 ].…”

Curcumin Mitigated TCE-induced Toxicity of A549 cell by Regulating Oxidative Stress and Apoptosis

“…Trichloroethylene (TCE) is an occupational high-risk poison and many workers die from TCE occupational hazards every year due to its widespread use [20]. The toxicity of TCE to cells is mainly caused by intracellular oxidative stress, which in turn leads to oxidative damage to cells and eventually leads to cell death [8]. Curcumin, as a natural compound, has been confirmed to have various pharmacological activities such as anti-inflammatory, antioxidant, and anti-tumor [21,22].…”

“…The risk of TCE on human health aroused widespread concern and its toxicity has been recognized and welldocumented [5]. TCE exposure can lead to numerous types of diseases, such as renal tubular injury, renal tubular epithelial cell necrosis, liver damage, especially respiratory disease (asthma, chronic bronchitis, rhinitis) [6][7][8].…”