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Effects of the Particulate Matter2.5 (PM2.5) on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity
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  • Journal title : Molecules and Cells
  • Volume 38, Issue 12,  2015, pp.1096-1104
  • Publisher : Korea Society for Molecular and Cellular Biology
  • DOI : 10.14348/molcells.2015.0194
 Title & Authors
Effects of the Particulate Matter2.5 (PM2.5) on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity
Kim, Jae-Yong; Lee, Eun-Young; Choi, Inho; Kim, Jihoe; Cho, Kyung-Hyun;
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Particulate () is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous solution on lipoprotein metabolism. Collected from Seoul, Korea was dissolved in water, and the water extract (final 3 and 30 ppm) was treated to human serum lipoproteins, macrophages, and dermal cells. extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared. treatment (final 30 ppm) also induced cellular uptake of oxidized LDL (oxLDL) into macrophages, especially in the presence of fructose (final 50 mM). Uptake of oxLDL along with production of reactive oxygen species was accelerated by solution in a dose-dependent manner. Further, solution caused cellular senescence in human dermal fibroblast cells. Microinjection of solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.
embryo;glycation;lipoprotein;oxidation;particulate matter 2.5;zebrafish;
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Becerra, T.A., Wilhelm, M., Olsen, J., Cockburn, M., and Ritz, B. (2013). Ambient air pollution and autism in Los Angeles county, California. Environ. Health Perspect 121, 380-386.

Bozlaker, A., Spada, N.J., Fraser, M.P., and Chellam, S. (2014). Elemental characterization of PM2.5 and PM10 emitted from light duty vehicles in the Washburn Tunnel of Houston, Texas: release of rhodium, palladium, and platinum. Environ. Sci. Technol. 48, 54-62. crossref(new window)

Brook, R.D., Rajagopalan, S., Pope, C.A. 3rd., Brook, J.R., Bhatnagar, A., Diez-Roux, A.V., Holguin, F., Hong, Y., Luepker, R.V., Mittleman, M.A., et al. (2010). Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation 121, 2331-2378. crossref(new window)

Chay, K., Dopkin, C., and Greenstone, M. (2003). The clean air act of 1970 and adult mortality. J. Risk Uncertainty 27, 279-300. crossref(new window)

Cho, K.H. (2009). Biomedicinal implications of high-density lipoprotein: its composition, structure, functions, and clinical applications. BMB Rep. 42, 393-400. crossref(new window)

Cho, K.H. (2011). Enhanced delivery of rapamycin by V156K apoAI high-density lipoprotein inhibits cellular pro-atherogenic effects and senescence and promotes tissue regeneration. J. Gerontol. A. Biol. Sci. Med. Sci. 66, 1274-1285.

Groop, P.H., Thomas, M.C., Rosengard-Barlund, M., Mills, V., Ronnback, M., Thomas, S., Forsblom, C., Taskinen, M.R., and Viberti, G. (2007). HDL composition predicts new-onset cardiovascular disease in patients with type 1 diabetes. Diabetes Care 30, 2706-2707. crossref(new window)

Jalava, P.I., Salonen, R.O., Pennanen, A.S., Happo, M.S., Penttinen, P., Halinen, A.I., Sillanpaa, M., Hillamo, R., and Hirvonen, M.R. (2008). Effects of solubility of urban air fine and coarse particles on cytotoxic and inflammatory responses in RAW 264.7 macrophage cell line. Toxicol. Appl. Pharmacol. 229, 146-160. crossref(new window)

Jang, W., Jeoung, N.H., and Cho, K.H. (2011). Modified apolipoprotein (apo) A-I by artificial sweetener causes severe premature cellular senescence and atherosclerosis with impairment of functional and structural properties of apoA-I in lipid-free and lipid-bound state. Mol. Cells 31, 461-470. crossref(new window)

Jin, S., and Cho, K.H. (2011). Water extracts of cinnamon and clove exhibits potent inhibition of protein glycation and antiatherosclerotic activity in vitro and in vivo hypolipidemic activity in zebrafish. Food Chem. Toxicol. 49, 1521-1529. crossref(new window)

Kim, J.Y., Kim, H.H., and Cho, K.H. (2013). Acute cardiovascular toxicity of sterilizers, PHMG, and PGH: severe inflammation in human cells and heart failure in zebrafish. Cardiovasc. Toxicol. 13, 148-160. crossref(new window)

Kim, J.Y., Park, K.H., Kim, J., Choi, I., and Cho, K.H. (2015a). Modified high-density lipoproteins by artificial sweetener, aspartame, and saccharin, showed loss of anti-atherosclerotic activity and toxicity in zebrafish. Cardiovasc. Toxicol. 15, 79-89. crossref(new window)

Kim, S.M., Lim, S.M., Yoo, J.A., Woo, M.J., and Cho, K.H. (2015b). Consumption of high-dose vitamin C (1,250 mg/day) enhances functional and structural properties of serum lipoprotein to improve anti-oxidant, anti-atherosclerotic, and anti-aging effects via regulation of anti-inflammatory microRNA. Food Funct. 6, 3604-3612. crossref(new window)

Nurkiewicz, T.R., Porter, D.W., Hubbs, A.F., Stone, S., Moseley, A.M., Cumpston, J.L., Goodwill, A.G., Frisbee, S.J., Perrotta, P.L., Brock, R.W., et al. (2011). Pulmonary particulate matter and systemic microvascular dysfunction. Res. Rep. Health Eff. Inst. 164, 3-48.

Nusslein-Volhard, C., and Dahm, R. (2002). Zebrafish: a practical approach. (New York: Oxford University Press).

Park, K.H., Shin, D.G., Kim, J.R., and Cho, K.H. (2010). Senescence-related truncation and multimerization of apolipoprotein A-I in high-density lipoprotein with an elevated level of advanced glycated end products and cholesteryl ester transfer activity. J. Gerontol. A. Biol. Sci. Med. Sci. 65, 600-610.

Park, K.H., and Cho, K.H. (2011a). A zebrafish model for the rapid evaluation of pro-oxidative and inflammatory death by lipopolysaccharide, oxidized low-density lipoproteins, and glycated highdensity lipoproteins. Fish Shellfish Immunol. 31, 904-910. crossref(new window)

Park, K.H., and Cho, K.H. (2011b). High-density lipoprotein (HDL) from elderly and reconstituted HDL containing glycated apolipoproteins A-I share proatherosclerotic and prosenescent properties with increased cholesterol influx. J. Gerontol. A. Biol. Sci. Med. Sci. 66, 511-520.

Park, K.H., Kim, J.M., and Cho, K.H. (2014a). Elaidic acid (EA) generates dysfunctional high-density lipoproteins and consumption of EA exacerbates hyperlipidemia and fatty liver change in zebrafish. Mol. Nutr. Food Res. 58, 1537-1545. crossref(new window)

Park, K.H., Shin, D.G., and Cho, K.H. (2014b). Dysfunctional lipoproteins from young smokers exacerbate cellular senescence and atherogenesis with smaller particle size and severe oxidation and glycation. Toxicol. Sci. 140, 16-25. crossref(new window)

Peng, R.D., Dominici, F., and Louis, T.A. (2006). Model choice in time series studies of air pollution and mortality. J. R. Statist. Soc. A. 169, 179-203. crossref(new window)

Peters, A., Dockery, D.W., Muller, J.E., and Mittleman, M.A. (2001). Increased particulate air pollution and the triggering of myocardial infarction. Circulation 103, 2810-2815. crossref(new window)

Pope, C.A.3rd., Burnett, R.T., Thurston, G.D., Thun, M.J., Calle, E.E., Krewski, D., and Godleski, J.J. (2004). Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease. Circulation 109, 71-77.

Ramos de Rainho, C., Machado Correa, S., Luiz Mazzei, J., Alessandra Fortes Aiub, C., and Felzenszwalb, I. (2013). Genotoxicity of polycyclic aromatic hydrocarbons and nitro-derived in respirable airborne particulate matter collected from urban areas of Rio de Janeiro (Brazil). Biomed. Res. Int. 2013, 765352.

Sun, Q., Yue, P., Deiuliis, J.A., Lumeng, C.N., Kampfrath, T., Mikolaj, M.B., Cai, Y., Ostrowski, M.C., Lu, B., Parthasarathy, S., et al. (2009). Ambient air pollution exaggerates adipose inflammation and insulin resistance in a mouse model of diet-induced obesity. Circulation 119, 538-546. crossref(new window)

Traversi, D., Schiliro, T., Degan, R., Pignata, C., Alessandria, L., and Gilli, G. (2011). Involvement of nitro-compounds in the mutagenicity of urban Pm2.5 and Pm10 in Turin. Mutat. Res. 726, 54-59. crossref(new window)

van Leuven, S.I., Stroes, E.S., and Kastelein, J.J. (2008). Highdensity lipoprotein: A fall from grace? Ann. Med. 40, 584-593. crossref(new window)

Volk, H.E., Lurmann, F., Penfold, B., Hertz-Picciotto, I., and McConnell, R. (2013). Traffic-related air pollution, particulate matter, and autism. JAMA Psychiatry 70, 71-77. crossref(new window)

Yoon, J.H., and Cho, K.H. (2012). A Point Mutant of Apolipoprotein A-I (V156K) Showed Enhancement of Cellular Insulin Secretion and Potent Activity of Facultative Regeneration in Zebrafish. Rejuvenation Res. 15, 313-321. crossref(new window)

Yoo, J.A., Lee, E.Y., Park, J.Y., Lee, S.T., Ham, S., and Cho, K.H. (2015). Different functional and structural characteristics between apoA-I and apoA-4 in lipid-free and reconstituted HDL state: apoA-4 showed less anti-atherogenic activity. Mol. Cells 38, 573-579. crossref(new window)