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Effects of the Particulate Matter₂.₅ (PM₂.₅) on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity.

Kim JY, Lee EY, Choi I, Kim J, Cho KH - Mol. Cells (2015)

Bottom Line: In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism.PM2.5 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.In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

View Article: PubMed Central - PubMed

Affiliation: School of Biotechnology, Korea.

ABSTRACT
Particulate matter2.5 (PM2.5) is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which PM2.5 aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism. Collected PM2.5 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. PM2.5 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. PM2.5 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 PM2.5 solution in a dose-dependent manner. Further, PM2.5 solution caused cellular senescence in human dermal fibroblast cells. Microinjection of PM2.5 solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

No MeSH data available.


Related in: MedlinePlus

Survivability of embryo in water containing PM2.5 water extract. (A) Survival graph of waterborne exposure to PM2.5 and LPS for 120 h. (B) Representative photo of embryos from stereoscopy and fluorospectroscopy. Impairment of skeletal development was observed by stereospectroscopy.
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f5-molce-38-12-1096: Survivability of embryo in water containing PM2.5 water extract. (A) Survival graph of waterborne exposure to PM2.5 and LPS for 120 h. (B) Representative photo of embryos from stereoscopy and fluorospectroscopy. Impairment of skeletal development was observed by stereospectroscopy.

Mentions: Waterborne exposure to PM2.5 in the presence of LPS (final 20 ppm) resulted in rapid death of zebrafish embryos in a dose-dependent manner (Fig. 5A). Embryos exposed to 3 and 30 ppm of PM2.5 solution for 120 h showed 80% and 65% survivability, respectively, whereas embryos treated with LPS alone and blank showed 95% and 100% survivability. As shown in Fig. 6, content in the embryo abdomen, a marker of developmental speed, was significantly reduced by 48% and 60% upon exposure to 3 and 30 ppm of PM2.5, respectively, compared to the control. These results suggest that embryonic survivability was more dependent on PM2.5 rather than LPS, a ubiquitous serum endotoxin. Developmental speed, as determined by melanin content, was attenuated upon exposure to PM2.5 in a dose-dependent manner.


Effects of the Particulate Matter₂.₅ (PM₂.₅) on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity.

Kim JY, Lee EY, Choi I, Kim J, Cho KH - Mol. Cells (2015)

Survivability of embryo in water containing PM2.5 water extract. (A) Survival graph of waterborne exposure to PM2.5 and LPS for 120 h. (B) Representative photo of embryos from stereoscopy and fluorospectroscopy. Impairment of skeletal development was observed by stereospectroscopy.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4697001&req=5

f5-molce-38-12-1096: Survivability of embryo in water containing PM2.5 water extract. (A) Survival graph of waterborne exposure to PM2.5 and LPS for 120 h. (B) Representative photo of embryos from stereoscopy and fluorospectroscopy. Impairment of skeletal development was observed by stereospectroscopy.
Mentions: Waterborne exposure to PM2.5 in the presence of LPS (final 20 ppm) resulted in rapid death of zebrafish embryos in a dose-dependent manner (Fig. 5A). Embryos exposed to 3 and 30 ppm of PM2.5 solution for 120 h showed 80% and 65% survivability, respectively, whereas embryos treated with LPS alone and blank showed 95% and 100% survivability. As shown in Fig. 6, content in the embryo abdomen, a marker of developmental speed, was significantly reduced by 48% and 60% upon exposure to 3 and 30 ppm of PM2.5, respectively, compared to the control. These results suggest that embryonic survivability was more dependent on PM2.5 rather than LPS, a ubiquitous serum endotoxin. Developmental speed, as determined by melanin content, was attenuated upon exposure to PM2.5 in a dose-dependent manner.

Bottom Line: In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism.PM2.5 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.In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

View Article: PubMed Central - PubMed

Affiliation: School of Biotechnology, Korea.

ABSTRACT
Particulate matter2.5 (PM2.5) is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which PM2.5 aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism. Collected PM2.5 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. PM2.5 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. PM2.5 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 PM2.5 solution in a dose-dependent manner. Further, PM2.5 solution caused cellular senescence in human dermal fibroblast cells. Microinjection of PM2.5 solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

No MeSH data available.


Related in: MedlinePlus