7-Dehydrocholesterol(7-DHC)은 콜레스테롤과 비타민 D의 전구물질로 피부가 자외선 B(UVB)에 노출되면 비타민 D3로 전환된다. 7-Dehydrocholesterol은 지질 과산화를 방지해서 세포를 보호하는 철사멸을 억제하는 천연 대사물질이다. 7-Dehydrocholesterol은 DHCR7 유전자 돌연변이로 인한 Smith-Lemli-Opitz 증후군(SLOS)에서 축적되는데 조직과 체액 중 콜레스테롤 수치가 낮고 소두증, 지적 장애 그리고 독특한 신체 특징을 특징으로 하는 질병이다[4, 5]. 7-Dehydrocholesterol은 인간 사이토크롬 P450 7A1(CYP7A1)에 의해 7-케토콜레스테롤로 전환될 수 있다[6].
References:
[1] Lehmann B, Genehr T, Knuschke P, et al. UVB-induced conversion of 7-dehydrocholesterol to 1α, 25-dihydroxyvitamin D3 in an in vitro human skin equivalent model[J]. Journal of investigative dermatology, 2001, 117(5): 1179-1185.
[2] Shin M H, Lee Y, Kim M K, et al. UV increases skin-derived 1α, 25-dihydroxyvitamin D3 production, leading to MMP-1 expression by altering the balance of vitamin D and cholesterol synthesis from 7-dehydrocholesterol[J]. The Journal of Steroid Biochemistry and Molecular Biology, 2019, 195: 105449.
[3] Li Y, Ran Q, Duan Q, et al. 7-Dehydrocholesterol dictates ferroptosis sensitivity[J]. Nature, 2024, 626(7998): 411-418.
[4] Waterham H R, Wanders R J A. Biochemical and genetic aspects of 7-dehydrocholesterol reductase and Smith-Lemli-Opitz syndrome[J]. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 2000, 1529(1-3): 340-356.
[5] Bianconi S E, Cross J L, Wassif C A, et al. Pathogenesis, epidemiology, diagnosis and clinical aspects of Smith–Lemli–Opitz syndrome[J]. Expert opinion on orphan drugs, 2015, 3(3): 267-280.
[6] Shinkyo R, Xu L, Tallman K A, et al. Conversion of 7-dehydrocholesterol to 7-ketocholesterol is catalyzed by human cytochrome P450 7A1 and occurs by direct oxidation without an epoxide intermediate[J]. Journal of Biological Chemistry, 2011, 286(38): 33021-33028.