عنوان
پدید آورنده
موضوع
رده
کتابخانه
محل استقرار
شماره کتابشناسی ملی
شماره
TL4f3544nf
زبان اثر
زبان متن نوشتاري يا گفتاري و مانند آن
انگلیسی
عنوان و نام پديدآور
عنوان اصلي
8-Week Inhalation of Ambient Particulate Matter with Distinct Chemical Signatures Differentially Alters Murine Cardiac Electrophysiology
نام عام مواد
[Thesis]
نام نخستين پديدآور
Herman, David Alexander
نام ساير پديدآوران
Kleinman, Michael T; Phalen, Robert F
وضعیت نشر و پخش و غیره
نام ناشر، پخش کننده و غيره
UC Irvine
تاریخ نشرو بخش و غیره
2020
یادداشتهای مربوط به پایان نامه ها
کسي که مدرک را اعطا کرده
UC Irvine
امتياز متن
2020
یادداشتهای مربوط به خلاصه یا چکیده
متن يادداشت
Introduction: Chronic exposure to particulate matter (PM) has been associated with increased risks for several cardiovascular (CV) diseases which can culminate in higher morbidity and mortality. This research will test the effects of particle chemistry on the mouse electrocardiogram (ECG) by investigating adverse cardiac outcomes following exposures 1) during different seasons (winter/summer), and 2) to whole concentrated ambient particle (CAPs; containing organic species) or denuded CAPs (DeCAPs; PM thermally stripped of organic species) with/without the addition of ozone (O3), a ubiquitous environmental pollutant. Methods: A Versatile Aerosol Concentration Enrichment System (VACES) was used to concentrated PM atmospheres. Hyperlipidemic mice (apoE-/-) were exposed via whole body inhalation chambers for 5 hrs./day, 4 days/wk. All ECG parameters were acquired from freely moving, conscious mice and assessed at the same time every evening. An aerosol mass spectrometer (AMS) provided single-particle size and chemical composition as well as cumulative size-classified mass concentrations in real-time for non-refractory sub-micron aerosol particles. The oxidative potential of different types of PM was analyzed using the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR). Results: Electrocardiogram (ECG) anomalies were exacerbated during periods with high ambient O3 levels suggesting that increased atmospheric interaction with O3 and other atmospheric pollutants generates more biologically active PM. CAPs exposure was found to be more cardiotoxic than DeCAPs exposure. Adding O3 to either CAPs or DeCAPs failed to elicit more severe adverse health effects compared to single pollutant exposures. Particles containing semi-volatile organic compounds (SVOCs) produced dissimilar inhibitory responses in GPx and GR suggesting that oxidative stress could be altered via GSH accumulation. Levels of enzymatic impairment were similar in response to PM+O3 mixtures regardless of PM-bound SVOCs present suggesting that O3 is reacting with a more stable PM-bound constituents.Conclusion: This report describes how inhaled ambient PM is linked to alterations in cardiac electrophysiology and provides useful insight into particle characterization and cardiac dysfunction in relation to specific PM fractions and/or PM+O3 mixtures. Information about particle oxidative stress would be a valued addition to air quality legislation which currently relies on particle size as a main toxicological risk factor.
نام شخص به منزله سر شناسه - (مسئولیت معنوی درجه اول )
مستند نام اشخاص تاييد نشده
Herman, David Alexander
نام شخص - ( مسئولیت معنوی درجه دوم )
مستند نام اشخاص تاييد نشده
Kleinman, Michael T; Phalen, Robert F
شناسه افزوده (تنالگان)
مستند نام تنالگان تاييد نشده
UC Irvine
دسترسی و محل الکترونیکی
نام الکترونيکي
مطالعه متن کتاب وضعیت انتشار
فرمت انتشار
p
اطلاعات رکورد کتابشناسی
نوع ماده
[Thesis]
کد کاربرگه
276903
اطلاعات دسترسی رکورد
سطح دسترسي
a
تكميل شده
Y
