Related Experiment Video
Updated: Jun 17, 2026
Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
Published on: February 7, 2018
Bilirubin Exerts Protective Effects on Alveolar Type II Pneumocytes in an In Vitro Model of Oxidative Stress
Stefanie Endesfelder1, Thomas Schmitz1, Christoph Bührer1
1Department of Neonatology, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.
Insights
Newborn infants experience high oxygen and bilirubin levels. Low-dose bilirubin protects rat alveolar epithelial cells (AEC II) from oxidative stress, suggesting a potential protective role.
Area of Science:
- Neonatal Physiology
- Cellular Biology
- Toxicology
Background:
- Newborns face rapid oxygen increase and rising unconjugated bilirubin levels.
- Bilirubin exhibits antioxidant properties but can also be toxic.
- Alveolar epithelial cells type II (AEC II) are crucial for lung function.
Purpose of the Study:
- To investigate AEC II responses to bilirubin under varying oxygen concentrations.
- To determine bilirubin's toxic threshold and its effects on cell viability.
- To explore bilirubin's impact on apoptosis and gene expression related to cell death and redox signaling.
Main Methods:
- Cell viability assays to establish bilirubin's toxic threshold.
- Incubation of rat AEC II with bilirubin under 5%, 21%, and 80% oxygen.
- Analysis of apoptosis induction and gene expression of redox-sensitive transcription factors (Nrf2, Hif1α, NFκB).
Main Results:
- Oxidative stress increased cell death and induced redox-sensitive signaling pathways.
- At 400 nm, bilirubin attenuated oxidative stress-induced cell death.
- Bilirubin modulated Nrf2/Hif1α- and NFκB-mediated signaling pathways.
Conclusions:
- Rat AEC II cells are protected from oxidative stress by low-dose bilirubin.
- Bilirubin may mediate cellular antioxidant defense in AEC II.
- Findings suggest a potential protective role for bilirubin in neonatal lung physiology.
Abstract:
Newborn infants face a rapid surge of oxygen and a more protracted rise of unconjugated bilirubin after birth. Bilirubin has a strong antioxidant capacity by scavenging free radicals, but it also exerts direct toxicity. This study investigates whether cultured rat alveolar epithelial cells type II (AEC II) react differently to bilirubin under different oxygen concentrations. The toxic threshold concentration of bilirubin was narrowed down by means of a cell viability test. Subsequent analyses of bilirubin effects under 5% oxygen and 80% oxygen compared to 21% oxygen, as well as pretreatment with bilirubin after 4 h and 24 h of incubation, were performed to determine the induction of apoptosis and the gene expression of associated transcripts of cell death, proliferation, and redox-sensitive transcription factors. Oxidative stress led to an increased rate of cell death and induced transcripts of redox-sensitive signaling pathways. At a non-cytotoxic concentration of 400 nm, bilirubin attenuated oxidative stress-induced responses and possibly mediated cellular antioxidant defense by influencing Nrf2/Hif1α- and NFκB-mediated signaling pathways. In conclusion, the study demonstrates that rat AEC II cells are protected from oxidative stress-induced impairment by low-dose bilirubin.
More Related Videos
10:00Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells
Published on: December 11, 2020
08:37Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer
Published on: November 15, 2024
