Hydrogen Water Protects Unborn Babies' Lungs from Infection Damage
- Authors
- Y. Hattori, T. Kotani, H. Tsuda, Y. Mano, L. Tu, H. Li, S. Hirako, T. Ushida, K. Imai, T. Nakano, Y. Sato, R. Miki, S. Sumigama, A. Iwase, S. Toyokuni, F. Kikkawa
- Journal
- Free Radical Research
- Year
- 2015
- DOI
- 10.3109/10715762.2015.1038257
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Fetal Lung Injury
- Body System
- Respiratory
TL;DR
Drinking hydrogen-rich water may help reduce lung damage in unborn babies when the mother experiences inflammation.
Key Finding
In pregnant rats exposed to an inflammatory trigger, maternal hydrogen water consumption reduced fetal lung cell damage, inflammation markers, and cell death compared to untreated pregnant rats.
Summary
This study examined whether hydrogen water could protect developing rat lungs from injury caused by maternal inflammation. Researchers exposed pregnant rats to an inflammatory trigger (lipopolysaccharide) and gave some mothers hydrogen water before the exposure. They found that mothers who drank hydrogen water had fetuses with less lung cell damage, less inflammation, and fewer signs of cell death compared to mothers who did not receive hydrogen water.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen water may help protect fetal lungs during maternal inflammation. However, these results are from rats only and have not been tested in humans, so it is too early to draw conclusions about whether this would work in pregnant women or affect premature infant health.
Abstract
Maternal inflammation is associated with spontaneous preterm birth and respiratory impairment among premature infants. Recently, molecular hydrogen (H2) has been reported to have a suppressive effect on oxidative stress and inflammation. The aim of this study was to evaluate the effects of H2 on fetal lung injury caused by maternal inflammation. Cell viability and the production of interleukin-6 (IL-6) and reactive oxygen species (ROS) were examined by treatment with lipopolysaccharide (LPS) contained in ordinal or H2-rich medium (HM) using a human lung epithelial cell line, A549. Pregnant Sprague Dawley rats were divided into three groups: Control, LPS, and HW + LPS groups. Rats were injected with phosphate-buffered saline (Control) or LPS intraperitoneally (LPS) on gestational day 19 and provided H2 water (HW) ad libitum for 24 h before LPS injection (HW + LPS). Fetal lung samples were collected on day 20, and the levels of apoptosis, oxidative damage, IL-6, and vascular endothelial growth factor (VEGF) were evaluated using immunohistochemistry. The number of apoptotic cells, and levels of ROS and IL-6 were significantly increased by LPS treatment, and repressed following cultured with HM in A549 cells. In the rat models, the population positive for cleaved caspase-3, 8-hydroxy-2'-deoxyguanosine, IL-6, and VEGF was significantly increased in the LPS group compared with that observed in the Control group and significantly decreased in the HW + LPS group. In this study, LPS administration induced apoptosis and oxidative damage in fetal lung cells that was ameliorated by maternal H2 intake. Antenatal H2 administration may decrease the pulmonary mobility associated with inflammation in premature infants.