# RF-006 — Reduced sperm function and oxidative DNA damage in vitro

Why this matters
Movement and DNA integrity matter to sperm function. This laboratory study of isolated human sperm reported impaired movement and survival, with DNA damage at higher exposures. It identifies specific reproductive endpoints worth examining, while leaving open whether comparable injury occurs in the body or affects fertility.

Id: RF-006

Author: De Iuliis et al.

Full Authors: Geoffry N. De Iuliis; Rhiannon J. Newey; Bruce V. King; R. John Aitken

Year: 2009

Title: Mobile Phone Radiation Induces Reactive Oxygen Species Production and DNA Damage in Human Spermatozoa In Vitro

Journal: plos one

Citation: De Iuliis GN, Newey RJ, King BV, Aitken RJ. Mobile Phone Radiation Induces Reactive Oxygen Species Production and DNA Damage in Human Spermatozoa In Vitro. PLoS ONE. 2009;4(7):e6446. doi:10.1371/journal.pone.0006446.

Doi: 10.1371/journal.pone.0006446

Pmid: 19649291

Topic: Reproduction

Verification Group: Original text reviewed

Record Role: Original text reviewed

Featured: True

Exposure: 1.8 GHz; 0.4-27.5 W/kg in vitro; 16 hours at 21 C.

Design: 22 normozoospermic donors supplied the sample pool. Figures 1-5 each use three biological replicates, per 2013 correction, not 22 independent replicates per SAR. Controls outside the waveguide;16 h at 21°C; separate heating experiment.

Finding: At 1 W/kg, human sperm vitality fell from 89% to 65% and motility from 86% to 68%. Oxidative DNA damage and fragmentation became significant at 2.8 W/kg and above.

Boundary: An in-vitro functional and DNA endpoint, not a human infertility incidence study. Culture SAR cannot be treated as a human local-SAR compliance test.

Related: RF-007 and RF-008 extend the Newcastle research lineage; not independent research networks.

Protection Question: Do the sperm changes seen in these culture conditions occur within the body and affect reproductive outcomes? Movement, viability and DNA integrity are relevant endpoints, but this isolated-cell experiment cannot establish infertility.

Access: Original full text and publisher correction independently rechecked.

Locator: Figures 2, 4 and 5; correction to Figure 1 and all figure legends

Notice: 2013 correction DOI 10.1371/annotation/9a8a0172-3850-4059-b852-72c330769c1b: Figures 1-5 n=3, not 4. Figure 1D mitochondrial ROS 28±1% exposed versus 5±1% control, P=.0056.

Funding: ARC Centre of Excellence in Biotechnology and Development CE0348239 and NHMRC Program Grant 494802; funders reported no role.

Conflicts: Authors declare no competing interests.

Source Url: https://doi.org/10.1371/journal.pone.0006446

Retrieval Links: https://doi.org/10.1371/journal.pone.0006446 | https://doi.org/10.1371/annotation/9a8a0172-3850-4059-b852-72c330769c1b | https://pubmed.ncbi.nlm.nih.gov/19649291/

Verification Date: 2026-10-20