Pathological Findings Observed in Kidneys of Postnatal Male Rats Exposed to 2100 MHz EMF
← Research streamCompared with controls, EMF-exposed groups showed deterioration of the brush border in renal tubules and more caspase-3-positive renal tubular epithelial cells. Kidney tissue MDA increased and GSH decreased in EMF groups versus control (reported p=0.00 for bo…
Study snapshot
Abstract
Pathological Findings Observed in Kidneys of Postnatal Male Rats Exposed to 2100 MHz EMF Bedir R, Tumkaya L, Mercantepe T, Yilmaz A. Pathological findings observed in the kidneys of postnatal male rats exposed to the 2100 MHz electromagnetic field. Arch Med Res. 2018 Dec 29. pii: S0188-4409(18)30433-8. doi: 10.1016/j.arcmed.2018.12.010. Abstract BACKGROUND: The widespread use by young people of modern communication devices such as mobile phones means that they are particularly exposed to electromagnetic fields (EMF) and other problems. However, few studies have researched the effects of long-term exposure to EMF in the kidney. We therefore investigated oxidative stress and apoptosis in long-term exposure to 2100 megahertz (MHz) in a rat model. MATERIALS AND METHODS: Twenty-four Sprague Dawley rats were divided into a control group (n = 8, no EMF exposure), a group exposed to 2100 MHz for 6 h for 30 d (n = 8), and a group exposed to 2100 MHz for12 h for 30 d (n = 8). Immunohistochemical analysis was performed, using caspase-3 to evaluate apoptosis. Immediately after treatment, reduced glutathione (GSH), malondialdehyde (MDA) in kidney tissue and serum levels of various biochemical compounds were measured to detect oxidative stress. RESULTS: Deterioration was observed in the brush border in renal tubules of the EMF groups. The results of the immunohistochemical analysis revealed a greater number of positively stained renal tubular epithelial cells in the EMF groups as compared with that in the control group. In the EMF groups, renal MDA levels increased, and renal GSH levels decreased compared with those in the control group, as shown by a biochemical examination (p = 0.00 and p = 0.00, respectively). CONCLUSION: The findings showed that exposure to 2100 MHz for 6 and 12 h induced oxidative stress-mediated acute renal injury, depending on the length of exposure and dosage. ncbi.nlm.nih.gov Excerpt The EMF groups were continually exposed to electromagnetic waves produced by an EMF generator (Anritsu MG3670B, Kanagawa, Japan) for 30 d, 6 and 12 h per day. The generator had a signal power of 3.47 mW (5.4 dBm) at 2100 MHz, which is similar to the level experienced in mobile phone talk mode. The whole body specific absorption rate (SAR) was calculated to be 0.024 W/kg ....
AI evidence extraction
Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.
Main findings
Compared with controls, EMF-exposed groups showed deterioration of the brush border in renal tubules and more caspase-3-positive renal tubular epithelial cells. Kidney tissue MDA increased and GSH decreased in EMF groups versus control (reported p=0.00 for both). Authors conclude 2100 MHz exposure for 6 or 12 h/day for 30 days induced oxidative stress-mediated acute renal injury, with effects depending on exposure duration/dose.
Outcomes measured
- Kidney histopathology (renal tubule brush border deterioration)
- Apoptosis marker (caspase-3 immunohistochemistry in renal tubular epithelial cells)
- Oxidative stress biomarkers in kidney tissue (MDA, GSH)
- Serum biochemical compounds (not specified)
Limitations
- No SAR/dosimetry details beyond whole-body SAR value provided in excerpt; local kidney SAR not reported
- Serum biochemical outcomes are mentioned but not specified in the abstract
- Only male rats studied; generalizability to humans not addressed in abstract
- Exposure system described as generator output similar to mobile phone talk mode, but real-world exposure patterns may differ
View raw extracted JSON
{
"study_type": "animal",
"exposure": {
"band": "RF",
"source": "EMF generator (mobile-phone-like 2100 MHz signal)",
"frequency_mhz": 2100,
"sar_wkg": 0.024,
"duration": "30 days; 6 h/day or 12 h/day"
},
"population": "Postnatal male Sprague Dawley rats",
"sample_size": 24,
"outcomes": [
"Kidney histopathology (renal tubule brush border deterioration)",
"Apoptosis marker (caspase-3 immunohistochemistry in renal tubular epithelial cells)",
"Oxidative stress biomarkers in kidney tissue (MDA, GSH)",
"Serum biochemical compounds (not specified)"
],
"main_findings": "Compared with controls, EMF-exposed groups showed deterioration of the brush border in renal tubules and more caspase-3-positive renal tubular epithelial cells. Kidney tissue MDA increased and GSH decreased in EMF groups versus control (reported p=0.00 for both). Authors conclude 2100 MHz exposure for 6 or 12 h/day for 30 days induced oxidative stress-mediated acute renal injury, with effects depending on exposure duration/dose.",
"effect_direction": "harm",
"limitations": [
"No SAR/dosimetry details beyond whole-body SAR value provided in excerpt; local kidney SAR not reported",
"Serum biochemical outcomes are mentioned but not specified in the abstract",
"Only male rats studied; generalizability to humans not addressed in abstract",
"Exposure system described as generator output similar to mobile phone talk mode, but real-world exposure patterns may differ"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"2100 MHz",
"RF-EMF",
"rat model",
"kidney",
"oxidative stress",
"malondialdehyde",
"glutathione",
"apoptosis",
"caspase-3",
"renal injury",
"SAR"
],
"suggested_hubs": [
{
"slug": "rf-animal-studies",
"weight": 0.9,
"reason": "Animal experiment assessing kidney outcomes after 2100 MHz RF exposure."
}
]
}AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.
Identifiers and source
DOI: 10.1016/j.arcmed.2018.12.010
PubMed: Not supplied
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