Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0849640 (
skin damage
)
1,516
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Methyl paraben (MP) is often used as a preservative in foods, drugs, and cosmetics because of its high reliability in safety based on the rapid excretion and nonaccumulation following administration. Light irradiation sometimes produces unexpected activity from chemicals such as MP; furthermore, there is ample opportunity for MP to be exposed to sunlight. Here, we investigated whether MP shows DNA damage after sunlight irradiation. Two major photoproducts, p-hydroxybenzoic acid (PHBA) and 3-hydroxy methyl paraben (MP-3OH), were detected after sunlight irradiation to an aqueous MP solution. Both photoproducts were inactive in the in vitro DNA damage assay that measures oxidized guanine formed in calf thymus DNA in the presence of divalent copper ion, a known mediator of oxidative DNA damage. Simulated MP metabolism using dermal tissues after light irradiation produced these two photoproducts, which reacted with a
microsomal
fraction (S9) of the skin. A metabolite from MP-3OH, not PHBA, caused distinct DNA damage in the in vitro assay. This active metabolite was identified as protocatechuic acid, a hydrolyzed MP-3OH product. In addition, NADH, a cellular reductant, enhanced DNA damage by approximately five times. These results suggest that reactive oxygen species generated by the redox cycle via metal ion and catechol autoxidation are participating in oxidative DNA damage. This study reveals that MP might cause
skin damage
involving carcinogenesis through the combined activation of sunlight irradiation and skin esterases.
...
PMID:Combined activation of methyl paraben by light irradiation and esterase metabolism toward oxidative DNA damage. 1865 63
Atmospheric particulate matter (PM) is an important cause of
skin damage
, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of
Ecklonia cava
Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of
E. cava
extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of
E. cava
extract or dieckol and analyzed for their viability, prostaglandin E
2
(PGE
2
) release, and gene expression of cyclooxygenase (COX)-1, COX-2,
microsomal
prostaglandin E
2
synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E
2
synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE
2
, and these changes were partially abrogated by
E. cava
extract.
E. cava
extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE
2
production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that
E. cava
extract and dieckol alleviate airborne PM10-induced PGE
2
production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus,
E. cava
extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM.
...
PMID:Marine Alga
Ecklonia cava
Extract and Dieckol Attenuate Prostaglandin E
2
Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter. 3123 5