Leszczynski D, Fagerholm S, Leszczynski K
Radiobiology Laboratory, Finnish Centre for Radiation and Nuclear Safety, Helsinki, Finland.
Photochem Photobiol. 1996 Dec;64(6):936-42. doi: 10.1111/j.1751-1097.1996.tb01858.x.
We examined the effects of broadband UVA radiation (320-400 nm) on a rat myeloid leukemia cell line-chloroma (ChL). A Phillips face tanner model HB 171/A was used as a light source. Chloroma were irradiated through a 5 mm thick glass filter that cut off all of the UVB contamination. The irradiances were measured, from 250 to 400 nm, with a well-characterized and calibrated double-grating spectroradiometer Optronic 742. The overall uncertainty of dose evaluation was estimated to be +/-15% (2 sigma). The cells were irradiated with UVA doses of 4 and 8 J/cm2 and cultured thereafter for 24 h. After this period of time, a marked decline up to 50% was observed in cell proliferation in UVA-irradiated ChL cultures. The cell proliferation decline was found to be caused by simultaneously occurring G2/M phase cell cycle arrest and apoptosis in part of the UVA-irradiated ChL population. Concomitantly, with the decline in cell proliferation, an increase was observed in the expression of the major histocompatibility (MHC) class I and II antigens. Because protein kinase C (PKC) is known to regulate cell proliferation, apoptosis and expression of MHC antigens, and because UVA was shown to regulate PKC activity/expression, we therefore examined whether UVA irradiation has any effect on the expression of isozymes of PKC. Western blots revealed that ChL express alpha, beta I, delta, epsilon, eta, and zeta/iota isozymes of PKC and that expression of all isozymes declined 24 h after UVA irradiation (8 J/cm2). Finally, PKC activation in ChL by exposure to phorbol ester caused cell cycle arrest in G1 phase but did not induce apoptosis. This suggests that the previously shown UVA-induced PKC activation in ChL might be responsible for the induction of MHC antigens but the simultaneously observed ChL apoptosis is likely to be mediated by PKC down-regulation. All together, our results suggest that UVA, at irradiance levels that resemble the outdoor exposure, may have profound effects on the immune-related properties of leukocytes. Thus, we speculate that in vivo the immune functions of leukocytes passing through dermal capillaries might be altered by exposure to solar UVA radiation.
我们研究了宽带UVA辐射(320 - 400纳米)对大鼠髓性白血病细胞系 - 绿色瘤(ChL)的影响。使用飞利浦面部美黑仪型号HB 171/A作为光源。通过一个5毫米厚的玻璃滤光片对绿色瘤细胞进行照射,该滤光片可滤除所有UVB污染。使用经过充分表征和校准的双光栅光谱辐射计Optronic 742测量250至400纳米范围内的辐照度。剂量评估的总体不确定度估计为±15%(2σ)。用4和8 J/cm²的UVA剂量照射细胞,然后培养24小时。在这段时间后,观察到UVA照射的ChL培养物中细胞增殖显著下降高达50%。发现细胞增殖下降是由部分UVA照射的ChL群体中同时发生的G2/M期细胞周期停滞和凋亡引起的。同时,随着细胞增殖的下降,主要组织相容性(MHC)I类和II类抗原的表达增加。因为已知蛋白激酶C(PKC)调节细胞增殖、凋亡和MHC抗原的表达,并且因为UVA被证明可调节PKC活性/表达,所以我们研究了UVA照射是否对PKC同工酶的表达有任何影响。蛋白质免疫印迹显示ChL表达PKC的α、βI、δ、ε、η和ζ/ι同工酶,并且在UVA照射(8 J/cm²)24小时后所有同工酶的表达均下降。最后,通过暴露于佛波酯使ChL中的PKC活化导致细胞周期停滞在G1期,但未诱导凋亡。这表明先前显示的ChL中UVA诱导的PKC活化可能是MHC抗原诱导的原因,但同时观察到的ChL凋亡可能是由PKC下调介导的。总之,我们的结果表明,在类似于户外暴露的辐照度水平下,UVA可能对白细胞的免疫相关特性产生深远影响。因此,我们推测在体内,穿过真皮毛细血管的白细胞的免疫功能可能会因暴露于太阳UVA辐射而改变。