Godar D E
Center for Devices and Radiological Health, Food and Drug Administration, Rockville, MD 20857, USA.
Photochem Photobiol. 1996 Jun;63(6):825-30. doi: 10.1111/j.1751-1097.1996.tb09638.x.
Equitoxic doses (10% clonogenic survival) of UV radiation (UVR) from the three waveband regions, i.e. UVA1 (340-400 nm), UVB (290-320 nm) and UVC (200-290 nm), were shown to induce immediate or delayed apoptosis in L5178Y-R murine lymphoma cells. Membrane and DNA damage were shown to be the most probable initiators of UVA1-induced immediate or UVR-induced delayed apoptosis, respectively. These UV-induced apoptotic processes appeared to utilize two different "core" biochemical mechanisms; however, one core mechanism could be initiated at two distinct sites (e.g. membrane or DNA) and result in disparate kinetics. In an attempt to resolve this mechanistic issue, the dependence on macromolecular synthesis of each UV-induced apoptotic mechanism was investigated. In the absence of UVR, inhibition of either transcription (actinomycin D) or translation (cycloheximide) induced apoptosis in a concentration- and time-dependent manner. These results suggest that an apoptotic mechanism exists that does not require macromolecular synthesis postinsult (constitutive). The UVR data demonstrate that UVA1-induced immediate apoptosis utilizes this constitutive mechanism (preprogrammed), while UVR-induced delayed apoptosis utilizes the well-known inducible mechanism (programmed). Therefore, there are two different core biochemical mechanisms of apoptotic death available to each cell: preprogrammed (constitutive) and programmed (inducible) cell death.
来自三个波段区域，即UVA1（340 - 400纳米）、UVB（290 - 320纳米）和UVC（200 - 290纳米）的等毒性剂量（克隆形成存活率为10%）的紫外线辐射（UVR），被证明可诱导L5178Y - R小鼠淋巴瘤细胞立即或延迟凋亡。膜损伤和DNA损伤分别被证明是UVA1诱导的立即凋亡或UVR诱导的延迟凋亡最可能的起始因素。这些紫外线诱导的凋亡过程似乎利用了两种不同的“核心”生化机制；然而，一种核心机制可以在两个不同的位点（如膜或DNA）启动，并导致不同的动力学。为了解决这个机制问题，研究了每种紫外线诱导的凋亡机制对大分子合成的依赖性。在没有UVR的情况下，转录抑制（放线菌素D）或翻译抑制（环己酰亚胺）以浓度和时间依赖性方式诱导凋亡。这些结果表明存在一种凋亡机制，其在损伤后不需要大分子合成（组成性）。UVR数据表明，UVA1诱导的立即凋亡利用这种组成性机制（预编程），而UVR诱导的延迟凋亡利用众所周知的诱导性机制（编程）。因此，每个细胞有两种不同的凋亡死亡核心生化机制：预编程（组成性）和编程（诱导性）细胞死亡。
