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Transcriptome analysis in mouse skin after exposure to ultraviolet radiation from a canopy sunbed. 小鼠皮肤暴露于天棚日光浴浴床紫外线辐射后的转录组分析。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-02-05 DOI: 10.1111/php.13917
Sami S Qutob, Samantha P M Roesch, Sandy Smiley, Pascale Bellier, Andrew Williams, Kate B Cook, Matthew J Meier, Andrea Rowan-Carroll, Carole L Yauk, James P McNamee

Exposure to ultraviolet radiation (UV-R), from both natural and artificial tanning, heightens the risk of skin cancer by inducing molecular changes in cells and tissues. Despite established transcriptional alterations at a molecular level due to UV-R exposure, uncertainties persist regarding UV radiation characterization and subsequent genomic changes. Our study aimed to mechanistically explore dose- and time-dependent gene expression changes, that may drive short-term (e.g., sunburn) and long-term actinic (e.g., skin cancer) consequences. Using C57BL/6N mouse skin, we analyzed transcriptomic expression following exposure to five erythemally weighted UV-R doses (0, 5, 10, 20, and 40 mJ/cm2) emitted by a UV-R tanning device. At 96 h post-exposure, 5 mJ/cm2 induced 116 statistically significant differentially expressed genes (DEGs) associated with structural changes from UV-R damage. The highest number of significant gene expression changes occurred at 6 and 48 h post-exposure in the 20 and 40 mJ/cm2 dose groups. Notably, at 40 mJ/cm2, 13 DEGs related to skin barrier homeostasis were consistently perturbed across all timepoints. UV-R exposure activated pathways involving oxidative stress, P53 signaling, inflammation, biotransformation, skin barrier maintenance, and innate immunity. This in vivo study's transcriptional data offers mechanistic insights into both short-term and potential non-threshold-dependent long-term health effects of UV-R tanning.

暴露于紫外线辐射(UV-R)(包括天然晒黑和人工晒黑)会诱导细胞和组织发生分子变化,从而增加患皮肤癌的风险。尽管已确定紫外线辐射会在分子水平上引起转录改变,但紫外线辐射的特征和随后的基因组变化仍存在不确定性。我们的研究旨在从机理上探索剂量和时间依赖性基因表达变化,这种变化可能会导致短期(如晒伤)和长期的光化学后果(如皮肤癌)。我们利用 C57BL/6N 小鼠皮肤,分析了暴露于紫外线日光浴设备发出的五种红斑加权紫外线剂量(0、5、10、20 和 40 mJ/cm2)后的转录组表达。暴露后 96 小时,5 mJ/cm2 诱导了 116 个具有统计学意义的差异表达基因(DEGs),这些基因与紫外线-R 损伤引起的结构变化有关。暴露后 6 小时和 48 小时,20 mJ/cm2 剂量组和 40 mJ/cm2 剂量组的重大基因表达变化数量最多。值得注意的是,在 40 mJ/cm2 剂量组中,13 个与皮肤屏障稳态有关的 DEGs 在所有时间点上都受到了持续干扰。紫外线照射激活了涉及氧化应激、P53 信号传导、炎症、生物转化、皮肤屏障维护和先天免疫的通路。这项体内研究的转录数据从机理上揭示了紫外线-R 晒黑对健康的短期影响和潜在的非阈值依赖性长期影响。
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引用次数: 0
Blue light impairs the repair of UVB-induced pyrimidine dimers in a human skin model. 在人体皮肤模型中,蓝光会损害紫外线诱导的嘧啶二聚体的修复。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-02-13 DOI: 10.1111/php.13921
Thierry Douki, Daniel Bacqueville, Carine Jacques, Camille Geniès, Nicolas Roullet, Sandrine Bessou-Touya, Hélène Duplan

In recent years, interest is growing in the biological cutaneous effects of high-energy visible light (400-450 nm). In the present study, we explored the impact of blue light (BL) on the repair of pyrimidine dimers, the major class of premutagenic DNA damage induced by exposure to sunlight. We unambiguously demonstrate that the exposure of in vitro reconstructed human epidermis to environmentally relevant doses of BL strongly decreases the rate of repair of cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts induced by a subsequent UVB irradiation. Using the highly sensitive and specific liquid chromatography-tandem mass spectrometry assay, we did not observe induction of pyrimidine dimers by BL alone. Finally, we showed that application, during the BL exposure step, of a formula containing a new filter, named TriAsorB and affording BL photoprotection, prevented the decrease in DNA repair efficiency. These results emphasize the potential deleterious effects of BL on DNA repair and the interest in providing adequate skin protection against this wavelength range of sunlight.

近年来,人们对高能可见光(400-450 nm)的皮肤生物效应越来越感兴趣。在本研究中,我们探讨了蓝光(BL)对嘧啶二聚体修复的影响,嘧啶二聚体是日光照射诱发的主要一类致突变前 DNA 损伤。我们明确地证明,将体外重建的人体表皮暴露于环境相关剂量的蓝光中,会大大降低环丁烷嘧啶二聚体和嘧啶(6-4)嘧啶酮光产物的修复率,而这些光产物是由随后的紫外线照射诱发的。利用高灵敏度和高特异性的液相色谱-串联质谱分析法,我们没有观察到 BL 单独诱导的嘧啶二聚体。最后,我们发现,在紫外线照射步骤中使用一种含有新型滤光器(名为 TriAsorB,具有紫外线光保护作用)的配方,可以防止 DNA 修复效率的降低。这些结果强调了碱性蓝光对 DNA 修复的潜在有害影响,以及针对这一波长范围的阳光提供充分的皮肤保护的重要性。
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引用次数: 0
Expression profiles and functional analysis of transfer RNA-derived small RNAs (tsRNAs) in photoaged human dermal fibroblasts. 转运核糖核酸衍生的小核糖核酸(tsRNA)在光老化的人类真皮成纤维细胞中的表达谱和功能分析。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-30 DOI: 10.1111/php.14015
Amin Yao, Yu Zhang, Mengting Ouyang, Lei Wen, Wei Lai

Transfer RNA-derived small RNAs (tsRNAs) refer to a newly established family of non-coding RNAs that regulate a diverse set of biological processes. However, the function of tsRNAs in skin photoaging remains unclear. This research aims to investigate the potential correlation between tsRNAs and skin photoaging. Human dermal fibroblasts (HDFs) were irradiated with UVA at 10 J/cm2 once a day lasting for 14 days, resulting in the establishment of a photoaging model induced by UVA. To identify the expression profiles and functions of tsRNAs, tsRNA sequencing and bioinformatics analysis were conducted. qPCR was employed to validate the results of differentially expressed (DE) tsRNAs. A total of 34 tsRNAs exhibited significant differential expression between the UVA and control groups (n = 3), with nine upregulated and 25 downregulated (log2 fold change >1.5, p-value <0.05). Six tsRNAs were selected at random and validated by qRT-PCR. The enrichment analysis of DE tsRNAs target genes indicated that the dysregulated tsRNAs appeared to be connected with cell cycle, DNA replication and the AGE-RAGE signaling pathway. The expression of tsRNAs was found to be aberrant in UVA-HDF. These findings provide insights into the UVA-induced damage and potential target genes for skin photoaging.

转运核糖核酸衍生小核糖核酸(tsRNAs)是新近建立的非编码核糖核酸家族,可调控多种生物过程。然而,tsRNAs 在皮肤光老化中的功能仍不清楚。本研究旨在探讨 tsRNAs 与皮肤光老化之间的潜在关联。用 10 J/cm2 的 UVA 照射人的真皮成纤维细胞(HDFs),每天一次,持续 14 天,从而建立由 UVA 诱导的光老化模型。为了确定tsRNA的表达谱和功能,研究人员进行了tsRNA测序和生物信息学分析。在 UVA 组和对照组(n = 3)之间,共有 34 个 tsRNAs 表现出显著的差异表达,其中 9 个上调,25 个下调(log2 对折变化 >1.5,p 值为 0.05)。
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引用次数: 0
Spectroscopic analysis of bacterial photoreactivation. 细菌光活化的光谱分析。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-29 DOI: 10.1111/php.14019
Keyvan Khosh Abady, Negar Karpourazar, Arjun Krishnamoorthi, Runze Li, Peter M Rentzepis

With the rise of bacterial infections and antibiotic resistance, spectroscopic devices originally developed for bacterial detection have shown promise to rapidly identify bacterial strains and determine the ratio of live to dead bacteria. However, the detection of the photoreactivated pathogens remains a critical concern. This study utilizes fluorescence and Raman spectroscopy to analyze bacterial responses to UV irradiation and subsequent photoreactivation. Our experimental results reveal limitations in fluorescence spectroscopy for detecting photoreactivated bacteria, as the intense fluorescence of tryptophan and tyrosine amino acids masks the fluorescence emitted by thymine molecules. Conversely, Raman spectroscopy proves more effective, showing a detectable decrease in band intensities of E. coli bacteria at 1248 and 1665 cm-1 after exposure to UVC radiation. Subsequent UVA irradiation results in the partial restoration of these band intensities, indicating DNA repair and bacterial photoreactivation. This enhanced understanding aims to improve the accuracy and effectiveness of these spectroscopic tools in clinical and environmental settings.

随着细菌感染和抗生素耐药性的增加,最初为细菌检测而开发的光谱设备在快速识别细菌菌株和确定活菌与死菌的比例方面大有可为。然而,对光活化病原体的检测仍然是一个关键问题。本研究利用荧光和拉曼光谱分析细菌对紫外线照射和随后的光氧化活化的反应。我们的实验结果揭示了荧光光谱在检测光活化细菌方面的局限性,因为色氨酸和酪氨酸氨基酸的强烈荧光会掩盖胸腺嘧啶分子发出的荧光。相反,拉曼光谱则更为有效,它显示大肠杆菌在受到紫外线辐射后,1248 和 1665 cm-1 处的带强度会出现可检测到的下降。随后的 UVA 照射导致这些波段强度部分恢复,表明 DNA 修复和细菌光复活。加深对这一现象的了解有助于提高这些光谱工具在临床和环境中的准确性和有效性。
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引用次数: 0
Impact of low-dose UV-A in Caenorhabditis elegans during candidate bacterial infections. 候选细菌感染期间低剂量紫外线 A 对草履虫的影响
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-28 DOI: 10.1111/php.14009
Balasubramanian Chellammal Muthubharathi, Pandiarajan Kaarmegam Subalakshmi, Bynedi Sheshatri Chinna Mounish, Toleti Subba Rao, Krishnaswamy Balamurugan

Ultraviolet radiation is a non-ionizing radiation produced by longer wavelength energy sources with lower frequency and is categorized into UV-A, UV-B, and UV-C. Minimal exposure to this radiation has several health benefits, which include treating microbial contaminations and skin therapies. However, the antimicrobial action of low-dose UV-A during pathogenic bacterial infections is still unrevealed. In this study, the impact of low-dose UV-A as pre- or post-treatment using the model organism, Caenorhabditis elegans with candidate pathogens (Acinetobacter baumannii and Staphylococcus aureus) mediated infections was investigated. The results indicated enrichment of metabolites, reduced level of antioxidants, increased expression of dopamine biosynthesis and transportation, and decrease in serotonin biosynthesis when the organism was exposed to low-dose UV-A for 5 min. This, in turn, elevated the expression of candidate regulatory proteins involved in lifespan determination, innate immunity, and cAMP-response element binding protein (CREB), which appear to increase the lifespan and brood size of C. elegans during A. baumannii and S. aureus infections. The findings suggested that the low-dose UV-A treatment during A. baumannii and S. aureus infections prolonged the lifespan and increased the egg-laying capacity of C. elegans.

紫外线辐射是一种非电离辐射,由波长较长、频率较低的能量源产生,分为紫外线 A、紫外线 B 和紫外线 C。微量暴露于这种辐射对健康有多种益处,包括治疗微生物污染和皮肤疗法。然而,低剂量 UV-A 在病原菌感染期间的抗菌作用仍未被揭示。在这项研究中,研究人员利用模型生物秀丽隐杆线虫与候选病原体(鲍曼不动杆菌和金黄色葡萄球菌)介导的感染,调查了低剂量紫外线-A 作为治疗前或治疗后的影响。结果表明,当生物体暴露于低剂量紫外线 A 5 分钟时,代谢物丰富,抗氧化剂水平降低,多巴胺生物合成和运输表达增加,血清素生物合成减少。这反过来又提高了涉及寿命决定、先天免疫和 cAMP 反应元件结合蛋白(CREB)的候选调控蛋白的表达,而这些蛋白似乎能在鲍曼不动杆菌和金黄色葡萄球菌感染期间增加秀丽隐杆线虫的寿命和育雏规模。研究结果表明,在鲍曼不动杆菌和金黄色葡萄球菌感染期间进行低剂量紫外线-A处理可延长秀丽隐杆线虫的寿命并提高其产卵能力。
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引用次数: 0
Trials and errors in the realm of photodynamic therapy: Viability and ROS detection. 光动力疗法领域的试验与失误:活力与 ROS 检测
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-27 DOI: 10.1111/php.14020
David Kessel

In the realm of Photodynamic Therapy, as elsewhere, claims are sometimes made for which there is minimal evidence or proof. Some examples are indicated.

在光动力疗法领域,与其他领域一样,有时也会出现证据或证明极少的说法。下面列举一些例子。
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引用次数: 0
Probing skin photoallergens in reconstructed human epidermis: An EPR spin trapping investigation. 在重建的人体表皮中探测皮肤光过敏原:EPR 自旋捕获研究
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-27 DOI: 10.1111/php.14010
Yannick Port-Lougarre, Guillaume Voegeli, Bertrand Vileno, Elena Giménez-Arnau

Photoallergic contact dermatitis is a skin disease caused by combined exposure to photoreactive chemicals and sunlight. Exposure to allergens and the risk of skin sensitization is an essential regulatory issue within the industry. Yet, only few non-validated assays for photoallergy assessment exist as the pathogenesis is not fully deciphered. Improving such assays and/or developing new ones require an understanding of the chemical mechanisms involved. The first key event in the photosensitization process, namely chemical binding of the photoallergen to endogenous proteins, is thought to proceed via photo-mediated radicals arising from the photoallergen. Moreover, the mechanism of action of these radicals if formed in the epidermis is not known and far from being unraveled. We present here an original proof-of-concept methodology to probe radical generation from allergens in contact with photoexposed skin, using electron paramagnetic resonance and spin trapping in a reconstructed human epidermis model mimicking real-life exposure scenarios.

光过敏性接触性皮炎是一种因接触光活性化学品和阳光而引起的皮肤病。接触过敏原和皮肤过敏风险是行业内一个重要的监管问题。然而,由于发病机理尚未完全破解,目前仅有少数未经验证的光过敏评估测定方法。要改进这些检测方法和/或开发新的检测方法,就必须了解其中涉及的化学机制。光敏过程中的第一个关键事件,即光过敏原与内源性蛋白质的化学结合,被认为是通过光过敏原产生的光自由基进行的。此外,如果这些自由基在表皮中形成,其作用机制尚不清楚,也远未解开。我们在此介绍一种新颖的概念验证方法,利用电子顺磁共振和自旋捕获技术,在模拟真实暴露场景的重建人体表皮模型中,探究过敏原与暴露皮肤接触后产生的自由基。
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引用次数: 0
Light exposure of tetra-cationic porphyrins containing peripheral Pd(II)-bipyridyl complexes and the induced effects on purified DNA molecule, fibroblast and melanoma cell lines. 含有外围钯(II)-联吡啶络合物的四阳离子卟啉的光照射及其对纯化 DNA 分子、成纤维细胞和黑色素瘤细胞系的诱导效应。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-27 DOI: 10.1111/php.14017
Luana B Trentin, Altevir R Viana, Sophia Iwersen, Bernardo A Iglesias, Otávio A Chaves, André P Schuch

Photodynamic therapy (PDT) combines a light source, oxygen, and a photosensitizer (PS) to generate reactive oxygen species (ROS) for treating diseases. In this study, we evaluated two meso-tetra-pyridyl porphyrins with [Pd(bpy)Cl]+, namely 3-PdTPyP and 4-PdTPyP, as PS for PDT application. DNA interaction was assessed by spectroscopic measurements (UV-Vis and fluorescence emission), viscosity analysis, and molecular docking simulations. The results indicate that Pd(II)-porphyrins do not intercalate into DNA, suggesting that the minor groove is the primary interaction site, mainly through van der Waals forces. These metalloporphyrins effectively induced nitrogenous bases oxidation, particularly in purines, after white light irradiation. The induced DNA lesions were able to inactivate plasmid DNA metabolism (DNA replication and transcription) in a bacterial model. 3-PdTPyP and 4-PdTPyP significantly decreased the viability of treated melanoma cell lines (A375 and B16-F10), demonstrating that melanoma cell lines were more sensitive to these Pd(II)-porphyrins than the fibroblast cell line (L929). Moreover, 3-PdTPyP was more photototoxic to A375 cells (IC50 = 0.43 μM), whereas 4-PdTPyP was more photototoxic to B16-F10 cells (IC50 = 0.51 μM). These findings suggest that these porphyrins are promising PS for future PDT research focused on skin cancer.

光动力疗法(PDT)将光源、氧气和光敏剂(PS)结合在一起,产生活性氧(ROS)来治疗疾病。在这项研究中,我们评估了两种含有 [Pd(bpy)Cl]+ 的介-四吡啶卟啉,即 3-PdTPyP 和 4-PdTPyP,作为光动力疗法应用的光敏剂。DNA 相互作用通过光谱测量(紫外可见光和荧光发射)、粘度分析和分子对接模拟进行了评估。结果表明,Pd(II)-卟啉不会插入 DNA,这表明小沟是主要的相互作用位点,主要通过范德华力作用。在白光照射下,这些金属卟啉能有效诱导含氮碱基氧化,尤其是嘌呤碱基氧化。诱导的 DNA 损伤能够使细菌模型中的质粒 DNA 代谢(DNA 复制和转录)失活。3-PdTPyP 和 4-PdTPyP 能显著降低经处理的黑色素瘤细胞系(A375 和 B16-F10)的存活率,表明黑色素瘤细胞系比成纤维细胞系(L929)对这些钯(II)卟啉更敏感。此外,3-PdTPyP 对 A375 细胞的光毒性更大(IC50 = 0.43 μM),而 4-PdTPyP 对 B16-F10 细胞的光毒性更大(IC50 = 0.51 μM)。这些研究结果表明,这些卟啉是很有希望用于未来以皮肤癌为重点的PDT研究的PS。
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引用次数: 0
PpIX-enabled fluorescence-based detection and photodynamic priming of platinum-resistant ovarian cancer cells under fluid shear stress. 在流体剪切应力作用下,对抗铂卵巢癌细胞进行基于 PpIX 的荧光检测和光动力诱导。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-27 DOI: 10.1111/php.14014
Mustafa Kemal Ruhi, Brittany P Rickard, Marta Overchuk, Prima Dewi Sinawang, Elizabeth Stanley, Matthew Mansi, Raymond G Sierra, Brandon Hayes, Xianming Tan, Demir Akin, Bin Chen, Utkan Demirci, Imran Rizvi

Over 75% percent of ovarian cancer patients are diagnosed with advanced-stage disease characterized by unresectable intraperitoneal dissemination and the presence of ascites, or excessive fluid build-up within the abdomen. Conventional treatments include cytoreductive surgery followed by multi-line platinum and taxane chemotherapy regimens. Despite an initial response to treatment, over 75% of patients with advanced-stage ovarian cancer will relapse and succumb to platinum-resistant disease. Recent evidence suggests that fluid shear stress (FSS), which results from the movement of fluid such as ascites, induces epithelial-to-mesenchymal transition and confers resistance to carboplatin in ovarian cancer cells. This study demonstrates, for the first time, that FSS-induced platinum resistance correlates with increased cellular protoporphyrin IX (PpIX), the penultimate downstream product of heme biosynthesis, the production of which can be enhanced using the clinically approved pro-drug aminolevulinic acid (ALA). These data suggest that, with further investigation, PpIX could serve as a fluorescence-based biomarker of FSS-induced platinum resistance. Additionally, this study investigates the efficacy of PpIX-enabled photodynamic therapy (PDT) and the secretion of extracellular vesicles under static and FSS conditions in Caov-3 and NIH:OVCAR-3 cells, two representative cell lines for high-grade serous ovarian carcinoma (HGSOC), the most lethal form of the disease. FSS induces resistance to ALA-PpIX-mediated PDT, along with a significant increase in the number of EVs. Finally, the ability of PpIX-mediated photodynamic priming (PDP) to enhance carboplatin efficacy under FSS conditions is quantified. These preliminary findings in monolayer cultures necessitate additional studies to determine the feasibility of PpIX as a fluorescence-based indicator, and mediator of PDP, to target chemoresistance in the context of FSS.

超过 75% 的卵巢癌患者被诊断为晚期疾病,其特点是无法切除的腹膜内播散和腹水(或腹腔内积液过多)。传统的治疗方法包括细胞切除手术,然后进行多线铂类和类固醇化疗。尽管对治疗有初步反应,但超过 75% 的晚期卵巢癌患者会因铂类耐药而复发和死亡。最近的证据表明,腹水等液体运动产生的流体剪切应力(FSS)会诱导上皮细胞向间质转化,并使卵巢癌细胞对卡铂产生耐药性。这项研究首次证明,FSS 诱导的铂抗性与细胞原卟啉 IX(PpIX)的增加有关,PpIX 是血红素生物合成的倒数第二种下游产物,使用临床批准的原药氨基乙酰丙酸(ALA)可提高其产量。这些数据表明,通过进一步研究,PpIX 可作为 FSS 诱导的铂耐药性的荧光生物标记物。此外,本研究还调查了在 Caov-3 细胞和 NIH:OVCAR-3 细胞(高分化浆液性卵巢癌(HGSOC)的两种代表性细胞系)中,PpIX 在静态和 FSS 条件下的光动力疗法(PDT)疗效和细胞外囊泡的分泌情况。FSS 可诱导细胞对 ALA-PpIX 介导的 PDT 产生抗性,同时 EVs 的数量也会显著增加。最后,还量化了在 FSS 条件下 PpIX 介导的光动力引物(PDP)增强卡铂疗效的能力。这些在单层培养物中的初步研究结果要求进行更多的研究,以确定 PpIX 作为基于荧光的指示剂和 PDP 的介导剂在 FSS 条件下针对化疗耐药性的可行性。
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引用次数: 0
Interventional human ocular safety experiments for 222-nm far-ultraviolet-C lamp irradiation. 222 纳米远紫外-C 灯照射的介入性人体眼部安全实验。
IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-19 DOI: 10.1111/php.14016
Kazunobu Sugihara, Sachiko Kaidzu, Masahiro Sasaki, Masaki Tanito

The study aimed to directly assess the ocular safety of 222-nm far-ultraviolet-C (UVC) irradiation in humans, given the limited clinical trials in this area. This wavelength offers the potential for safe and effective microbial inactivation in occupied spaces, but its safety profile for human eyes requires thorough investigation. This prospective, interventional study involved five subjects aged 29-47 years, who were exposed to 222-nm UVC at doses of 22, 50, and 75 mJ/cm2. The subjects were monitored using custom-made glasses with a UV-cut filter on one eye to serve as a control. UVC irradiation was conducted using a KrCl excimer lamp, and ocular examinations were performed prior to exposure, 24 h post-exposure, and at 1, 3, and 6 months. Parameters assessed included visual acuity, refractive error, corneal endothelial density, corneal erosion scores, and conjunctival hyperemia scores. The study found no clinically significant photokeratitis or long-term eye damage across the five subjects, even at the highest dose of 75 mJ/cm2. Temporary ocular discomfort, including sensations of dryness and epiphora, was reported, but these symptoms subsided within hours after irradiation. The findings indicate that 222-nm far-UVC irradiation up to 75 mJ/cm2 does not cause "clinically significant photokeratitis" or long-term ocular damage, though it may induce temporary discomfort. This supports the safe use of 222-nm UVC for germicidal applications in occupied environments, providing a basis for revised safety guidelines.

该研究旨在直接评估 222 纳米远紫外-C(UVC)辐照对人类眼睛的安全性,因为这方面的临床试验非常有限。这种波长可安全有效地灭活占用空间中的微生物,但其对人眼的安全性还需要深入研究。这项前瞻性干预研究涉及五名 29-47 岁的受试者,他们分别暴露在 222 纳米紫外线下,剂量分别为 22、50 和 75 mJ/cm2。受试者的一只眼睛作为对照,使用带有紫外线切割滤镜的定制眼镜进行监测。使用 KrCl 准分子灯进行紫外线照射,并在照射前、照射后 24 小时以及照射 1、3 和 6 个月时进行眼部检查。评估参数包括视力、屈光不正、角膜内皮密度、角膜糜烂评分和结膜充血评分。研究发现,即使使用 75 mJ/cm2 的最高剂量,五名受试者也没有出现明显的临床光角膜炎或长期眼损伤。有暂时性眼部不适的报告,包括干涩和眼球上睑下垂的感觉,但这些症状在照射后几小时内就消退了。研究结果表明,最高 75 mJ/cm2 的 222 纳米远紫外线辐照不会引起 "临床上明显的光角膜炎 "或长期的眼部损伤,尽管可能会引起暂时的不适。这支持在有人居住的环境中安全使用 222 纳米紫外线杀菌,为修订安全指南提供了依据。
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引用次数: 0
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Photochemistry and Photobiology
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