Ovarian Damages Produced by Aerosolized Fine Particulate Matter (PM2.5) Pollution in Mice

Gai, Hui-Fang; An, Jian-Xiong; Qian, Xiaoyan; Wei, Yongjie; Williams, John P.; Gao, Gan

doi:10.4103/0366-6999.207472

Cited by 52 publications

(26 citation statements)

References 47 publications

(50 reference statements)

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“…12 In the third study, mice treated with a PM 2.5 suspension (10 mg/kg), every 2 days, for 22 days had serum anti-Müllerian hormone levels that were decreased by more than half compared to the control group. 11 Furthermore, IL-6 and TNF-α concentrations and the number of apoptotic cells were increased in ovarian tissue and ovarian histologic structures showed evidence of hemorrhage and vascular congestion in mice exposed to PM 2.5 compared to the control group. 11 Taken together with our findings, these data suggest that exposure to PM 2.5 throughout adult life may enhance follicular atresia through effects on ovarian inflammation, oxidative stress, and apoptosis, even at exposure levels within the World Health Organization guidelines (e.g.…”

Section: Discussionmentioning

confidence: 89%

“…Animal studies suggest that increased exposure to PM 2.5 may compromise female reproductive potential by accelerating reproductive aging. [11][12][13] Therefore, to address this question in women, we investigated the association between estimated residential exposure to PM 2.5 and antral follicle counts, the gold standard measure of ovarian reserve, 14 among women presenting to an infertility clinic.…”

Section: Introductionmentioning

confidence: 99%

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Exposure to Fine Particulate Matter and Ovarian Reserve Among Women from a Fertility Clinic

et al. 2019

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Background.-An increasing number of studies have linked air pollution to decreased fertility. Whether this is due to an effect on ovarian reserve is unknown. Method.-Our study included 632 women attending the Massachusetts General Hospital Fertility Center (2004-2015) who had a measured antral follicle count. Validated spatiotemporal models estimated daily particulate matter <2.5 μg/m 3 (PM 2.5) (based on residential address) for the 3 months prior to the antral follicle count. We analyzed associations with Poisson regression. Results.-Every 2 μg/m 3 increase in estimated PM 2.5 exposure was associated with a −7.2% (95% CI −10.4%, −3.8%) lower antral follicle count adjusting for age, BMI, smoking status, and year and season of the count. The association of PM 2.5 with antral follicle count was stronger among women with female factor infertility (−16.3% per 2 μg/m 3).

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Exposure to Fine Particulate Matter and Ovarian Reserve Among Women from a Fertility Clinic

et al. 2019

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“…[ 1 ] Studies on electromagnetic radiation to the male reproductive system have focused on spermatogenesis,[ 2 ] testosterone,[ 3 ] and reactive oxygen species (ROS) in semen. [ 4 ] The complex defense system against electromagnetic radiation on the adverse effects of radiation-induced ROS includes enzymatic and nonenzymatic antioxidants, such as Vitamin C,[ 5 ] Vitamin E,[ 6 ] superoxide dismutase (SOD), and glutathione peroxidase (GSH-P X ). [ 7 ] Mailankot et al .,[ 8 ] Atasoy et al .,[ 9 ] and Esmekaya et al .…”

Section: Introductionmentioning

confidence: 99%

Moderate Dose of Trolox Preventing the Deleterious Effects of Wi-Fi Radiation on Spermatozoa In vitro through Reduction of Oxidative Stress Damage

Ding

Sun

Zhang

et al. 2018

Chinese Medical Journal

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Background:The worsening of semen quality, due to the application of Wi-Fi, can be ameliorated by Vitamin E. This study aimed to demonstrate whether a moderate dose of trolox, a new Vitamin E, inhibits oxidative damage on sperms in vitro after exposure to Wi-Fi radiation.Methods:Each of the twenty qualified semen, gathered from June to October 2014 in eugenics clinic, was separated into four aliquots, including sham, Wi-Fi-exposed, Wi-Fi plus 5 mmol/L trolox, and Wi-Fi plus 10 mmol/L trolox groups. At 0 min, all baseline parameters of the 20 samples were measured in sequence. Reactive oxygen species, glutathione, and superoxide dismutase were evaluated in the four aliquots at 45 and 90 min, as were sperm DNA fragments, sperm mitochondrial potential, relative amplification of sperm mitochondrial DNA, sperm vitality, and progressive and immotility sperm. The parameters were analyzed by one-way analysis of variance and Tukey's posttest.Results:Among Wi-Fi plus 5 mmol/L trolox, Wi-Fi-exposed and Wi-Fi plus 10 mmol/L trolox groups, reactive oxygen species levels (45 min: 3.80 ± 0.41 RLU·10−6·ml−1 vs. 7.50 ± 0.35 RLU·10−6·ml−1 vs. 6.70 ± 0.47 RLU·10−6·ml−1, P < 0.001; 90 min: 5.40 ± 0.21 RLU·10−6·ml−1 vs. 10.10 ± 0.31 RLU·10−6·ml−1 vs. 7.00 ± 0.42 RLU·10−6·ml−1, P < 0.001, respectively), percentages of tail DNA (45 min: 16.8 ± 2.0% vs. 31.9 ± 2.5% vs. 61.3 ± 1.6%, P < 0.001; 90 min: 19.7 ± 1.5% vs. 73.7 ± 1.3% vs. 73.1 ± 1.1%, P < 0.001, respectively), 8-hydroxy-2’-deoxyguanosine (45 min: 51.89 ± 1.46 pg/ml vs. 104.89 ± 2.19 pg/ml vs. 106.11 ± 1.81 pg/ml, P = 0.012; 90 min: 79.96 ± 1.73 pg/ml vs. 141.73 ± 2.90 pg/ml vs. 139.06 ± 2.79 pg/ml; P < 0.001), and percentages of immotility sperm (45 min: 27.7 ± 2.7% vs. 41.7 ± 2.2% vs. 41.7 ± 2.5%; 90 min: 29.9 ± 3.3% vs. 58.9 ± 4.0% vs. 63.1 ± 4.0%; all P < 0.001) were lowest, and glutathione peroxidase (45 min: 60.50 ± 1.54 U/ml vs. 37.09 ± 1.77 U/ml vs. 28.18 ± 1.06 U/ml; 90 min: 44.61 ± 1.23 U/ml vs. 16.86 ± 0.93 U/ml vs. 29.94 ± 1.56 U/ml; all P < 0.001), percentages of head DNA (45 min: 83.2 ± 2.0% vs. 68.2 ± 2.5% vs. 38.8 ± 1.6%; 90 min: 80.3 ± 1.5% vs. 26.3 ± 1.3% vs. 26.9 ± 1.1%; all P < 0.001), percentages of sperm vitality (45 min: 89.5 ± 1.6% vs. 70.7 ± 3.1% vs. 57.7 ± 2.4%; 90 min: 80.8 ± 2.2% vs. 40.4 ± 4.0% vs. 34.7 ± 3.9%; all P < 0.001), and progressive sperm (45 min: 69.3 ± 2.7% vs. 55.8 ± 2.2% vs. 55.4 ± 2.5%; 90 min: 67.2 ± 3.3% vs. 38.2 ± 4.0% vs. 33.9 ± 4.0%; all P < 0.001) were highest in Wi-Fi plus 5 mmol/L trolox group at 45 and 90 min, respectively. Other parameters were not affected, while the sham group maintained the baseline.Conclusion:This study found that 5 mmol/L trolox protected the Wi-Fi-exposed semen in vitro from the damage of electromagnetic radiation-induced oxidative stress.

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“…[ 3 ] In particular, heavy metal, polyaromatic hydrocarbons, and other toxic substances are readily adsorbed to PM 2.5 owing to its relatively small size and large surface area, which could reach some special biological sites and thereby lead to functional alteration, whereas larger PM cannot reach such sites. [ 4 5 6 ]…”

Section: Introductionmentioning

confidence: 99%

PM2.5 Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes

Hu¹,

Xie

Xu³

et al. 2017

Chinese Medical Journal

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Background:PM2.5 (aerodynamic diameter ≤ 2.5 μm) is a dominant and ubiquitous air pollutant that has become a global concern as PM2.5 exposure has been linked to many adverse health effects including cardiovascular and pulmonary diseases. Emerging evidence supports a correlation between increased air PM2.5 levels and skin disorders although reports on the underlying pathophysiological mechanisms are limited. Oxidative stress is the most common mechanism of PM2.5-induced adverse health effects. This study aimed to investigate PM2.5-induced oxidative damage and apoptosis in immortalized human keratinocyte (HaCaT) cells.Methods:HaCaT cells were exposed to 0, 25, 50, 100, or 200 μg/ml PM2.5 for 24 h. Reactive oxygen species (ROS) generation, lipid peroxidation products, antioxidant activity, DNA damage, apoptotic protein expression, and cell apoptosis were measured.Results:PM2.5 exposure (0–200 μg/ml) for 24 h resulted in increased ROS levels (arbitrary unit: 201.00 ± 19.28, 264.50 ± 17.91, 305.05 ± 19.57, 427.95 ± 18.32, and 436.70 ± 17.77) and malondialdehyde production (0.54 ± 0.05 nmol/mg prot, 0.61 ± 0.06 nmol/mg prot, 0.68 ± 0.05 nmol/mg prot, 0.70 ± 0.05 nmol/mg prot, and 0.76 ± 0.05 nmol/mg prot), diminished superoxide dismutase activity (6.47 ± 0.28 NU/mg prot, 5.97 ± 0.30 NU/mg prot, 5.15 ± 0.42 NU/mg prot, 4.08 ± 0.20 NU/mg prot, and 3.76 ± 0.37 NU/mg prot), and increased DNA damage and apoptosis in a dose-dependent manner in HaCaT cells. Moreover, cytochrome-c, caspase-3, and caspase-9 expression also increased proportionately with PM2.5 dosing.Conclusion:PM2.5 might elicit oxidative stress and mitochondria-dependent apoptosis that likely manifests as skin irritation and damage.

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Ovarian Damages Produced by Aerosolized Fine Particulate Matter (PM2.5) Pollution in Mice

Cited by 52 publications

References 47 publications

Exposure to Fine Particulate Matter and Ovarian Reserve Among Women from a Fertility Clinic

Exposure to Fine Particulate Matter and Ovarian Reserve Among Women from a Fertility Clinic

Moderate Dose of Trolox Preventing the Deleterious Effects of Wi-Fi Radiation on Spermatozoa In vitro through Reduction of Oxidative Stress Damage

PM2.5 Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes

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