17β-Estradiol Alters Rat Type-II Alveolar Cell Recovery from High Levels of Ozone

Abstract

Respiratory health is negatively impacted by exposure to ozone or to estrogens. Increasingly, individuals have simultaneous environmental exposure to both compounds. Characterizing the cellular responses stimulated by the combination of ozone and estrogens, therefore, is crucial to our complete understanding of the compounds' environmental health impacts. Our work introduces an alveolar cell culture model with defined media that provides evidence of ozone damage and determines sex hormones alter the cells' susceptibility to oxidative damage. Specifically, we investigated the individual and combined effects of environmentally relevant levels of ozone and 17β-estradiol on non-cancerous rat, type-II alveolar cells by examining biomarkers of cellular health and redox balance. The data reveal a complex role for 17β-estradiol in cellular recovery from 1 hr exposure to high ozone levels. At 0.5 hr post-ozone necrosis and inflammation markers show 17β-estradiol augments the detrimental effects of 350 ppb ozone, but after 24 hr of recovery, steroid treatment alters glutathione redox ratio and allows cellular proliferation.

High Ozone (O3) Affects the Fitness Associated with the Microbial Composition and Abundance of Q Biotype Bemisia tabaci

“…O 3 (≥200 ppb) has antimicrobial and deodorizing properties that make it useful in medicine, but as a major air pollutant, it has strong toxic effects on some organisms ( Mokoena et al, 2011 ). The EPA defined O 3 concentrations ≥350 ppb as hazardous to almost all organisms, and they can affect the survival and distribution of almost all organisms and break down the long-term sustainability of natural ecosystems ( Chalfant et al, 2011 ). In fact, in the forested regions of North America, the concentration of O 3 reached 200 ppb in Kress et al (1982) , and the maximum atmospheric concentration in Beijing was 273–477 ppb in July 2000 ( Wang and Cai, 2002 ; An et al, 2007 ), which was far beyond the mean global concentration (40 ppb) and the safe level (100 ppb) defined by the EPA.…”

Involvement of oxidative stress and impaired lysosomal degradation in amiodarone‐induced schwannopathy

“…The involvement of lipid peroxidation and oxidative stress in AMD cytotoxicity has recently been suggested (Durukan et al ., ; Lu et al ., ). In this study, AMD‐induced oxidative stress in IFRS1 cells was evaluated by the quantitation of the Nrf2 DNA‐binding activity (Ma, ) and glutathione redox state (GSH/GSSG) (Chalfant & Bernd, ). The Nrf2 activity in [AMD‐5 μ m ] (one‐way anova , F 3,12 = 8.25, P = 0.0273) and [AMD‐10 μ m ] ( F 3,12 = 8.25, P = 0.0188) was significantly (approximately twofold) higher than that in [Control] (Fig.…”

Improved hematopoietic differentiation of human pluripotent stem cells via estrogen receptor signaling pathway

“…E2 at 10 −8 M and 10 −7 M provided synergistic effects with hGFs on hematopoietic differentiation (Additional file 3 : Figure S2). E2 at 10 −8 M concentration was used for following experiments since it is physiologically more relevant [ 16 , 17 ]. As suggested by our previous report [ 15 ], hGFs exhibited a dramatic increase of hematopoietic progenitors (CD34 + CD45 + ) and mature blood (CD34 − CD45 + ) cells.…”