Mobile phone (1800MHz) radiation impairs female reproduction in mice through stress induced inhibition of ovarian & uterine activity
← Research streamCompared with controls, mice exposed to 1800 MHz mobile phone radiation (stand-by, dialing, receiving modes) showed increased oxidative/nitrosative stress markers and serum corticosterone with decreased antioxidant enzymes in hypothalamus, ovary, and uterus. …
Study snapshot
Abstract
Mobile phone (1800MHz) radiation impairs female reproduction in mice through stress induced inhibition of ovarian & uterine activity Shahin S, Singh SP, Chaturvedi CM. Mobile Phone (1800MHz) Radiation Impairs Female Reproduction in Mice, Mus musculus, through Stress Induced Inhibition of Ovarian and Uterine Activity. Reprod Toxicol. 2017 Aug 2. pii: S0890-6238(17)30167-3. doi: 10.1016/j.reprotox.2017.08.001. Highlights • Mice exposed to mobile phone radiation (MPR) in different operative modes. • Ovarian & uterine histopathology, steroidogenesis & stress parameters were checked. • Degenerative changes & reduced follicle count were observed in MPR exposed ovary. • MPR resulted significant decrease in ovarian steroidogenic proteins & sex steroids. • MPR induced oxidative & nitrosative stress impairs reproductive functions in mice. Abstract Present study investigated the long-term effects of mobile phone (1800MHz) radiation in stand-by, dialing and receiving modes on the female reproductive function (ovarian and uterine histo-architecture, and steroidogenesis) and stress responses (oxidative and nitrosative stress). We observed that mobile phone radiation induces significant elevation in ROS, NO, lipid peroxidation, total carbonyl content and serum corticosterone coupled with significant decrease in antioxidant enzymes in hypothalamus, ovary and uterus of mice. Compared to control group, exposed mice exhibited reduced number of developing and mature follicles as well as corpus lutea. Significantly decreased serum levels of pituitary gonadotrophins (LH, FSH), sex steroids (E2 and P4) and expression of SF-1, StAR, P-450scc, 3β-HSD, 17β-HSD, cytochrome P-450 aromatase, ER-α and ER-β were observed in all the exposed groups of mice, compared to control. These findings suggest that mobile phone radiation induces oxidative and nitrosative stress, which affects the reproductive performance of female mice. ncbi.nlm.nih.gov
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, mice exposed to 1800 MHz mobile phone radiation (stand-by, dialing, receiving modes) showed increased oxidative/nitrosative stress markers and serum corticosterone with decreased antioxidant enzymes in hypothalamus, ovary, and uterus. Exposed mice had reduced developing/mature follicles and corpus lutea, decreased serum LH/FSH and E2/P4, and reduced expression of multiple ovarian steroidogenic proteins and estrogen receptors.
Outcomes measured
- Ovarian histo-architecture/histopathology
- Uterine histo-architecture/histopathology
- Follicle count (developing and mature follicles)
- Corpus lutea count
- Oxidative stress markers (ROS, lipid peroxidation, total carbonyl content)
- Nitrosative stress marker (NO)
- Antioxidant enzyme levels
- Serum corticosterone
- Serum pituitary gonadotrophins (LH, FSH)
- Serum sex steroids (E2, P4)
- Expression of steroidogenic proteins/markers (SF-1, StAR, P-450scc, 3β-HSD, 17β-HSD, cytochrome P-450 aromatase)
- Estrogen receptor expression (ER-α, ER-β)
Limitations
- Sample size not reported in provided abstract/metadata
- Specific exposure metrics (e.g., SAR, power density) not reported in provided abstract/metadata
- Exposure duration not quantified beyond 'long-term' in provided abstract/metadata
View raw extracted JSON
{
"study_type": "animal",
"exposure": {
"band": "RF",
"source": "mobile phone",
"frequency_mhz": 1800,
"sar_wkg": null,
"duration": "long-term; stand-by, dialing and receiving modes"
},
"population": "Female mice (Mus musculus)",
"sample_size": null,
"outcomes": [
"Ovarian histo-architecture/histopathology",
"Uterine histo-architecture/histopathology",
"Follicle count (developing and mature follicles)",
"Corpus lutea count",
"Oxidative stress markers (ROS, lipid peroxidation, total carbonyl content)",
"Nitrosative stress marker (NO)",
"Antioxidant enzyme levels",
"Serum corticosterone",
"Serum pituitary gonadotrophins (LH, FSH)",
"Serum sex steroids (E2, P4)",
"Expression of steroidogenic proteins/markers (SF-1, StAR, P-450scc, 3β-HSD, 17β-HSD, cytochrome P-450 aromatase)",
"Estrogen receptor expression (ER-α, ER-β)"
],
"main_findings": "Compared with controls, mice exposed to 1800 MHz mobile phone radiation (stand-by, dialing, receiving modes) showed increased oxidative/nitrosative stress markers and serum corticosterone with decreased antioxidant enzymes in hypothalamus, ovary, and uterus. Exposed mice had reduced developing/mature follicles and corpus lutea, decreased serum LH/FSH and E2/P4, and reduced expression of multiple ovarian steroidogenic proteins and estrogen receptors.",
"effect_direction": "harm",
"limitations": [
"Sample size not reported in provided abstract/metadata",
"Specific exposure metrics (e.g., SAR, power density) not reported in provided abstract/metadata",
"Exposure duration not quantified beyond 'long-term' in provided abstract/metadata"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"1800 MHz",
"mobile phone radiation",
"female reproduction",
"mice",
"ovary",
"uterus",
"steroidogenesis",
"oxidative stress",
"nitrosative stress",
"corticosterone",
"LH",
"FSH",
"estradiol",
"progesterone"
],
"suggested_hubs": [
{
"slug": "animal-studies",
"weight": 0.9,
"reason": "Experimental study in mice assessing reproductive and stress outcomes after 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.reprotox.2017.08.001
PubMed: Not supplied
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