质体醌重组的D1／D2／Cytb559复合物的荧光衰减动力学和光破坏作用

光系统Ⅱ反应中心Ｄ１／Ｄ２／Ｃｙｔｂ５５９ 在分离纯化过程中失去了电子受体ＱＡ 和ＱＢ,人工合成的质体醌可以与Ｄ１／Ｄ２／Ｃｙｔｂ５５９ 复合物发生重组。癸基质体醌（ＤＰＱ）与Ｄ１／Ｄ２／Ｃｙｔｂ５９９ 复合物的重组导致该复合物的荧光强度下降及发射光谱蓝移,同时两个与光化学活性相关的长寿命（２４ ｎｓ和７３ ｎｓ）荧光衰减组分占整个荧光的百分数下降,这些结果表明ＤＰＱ作为Ｐｈｅｏ－ 的电子受体,限制了Ｐ６８０＋ ·Ｐｈｅｏ－ 的电荷重组。ＤＰＱ 的加入对Ｄ１／Ｄ２／Ｃｙｔｂ５５９复合物中Ｃｈｌａ 分子的光破坏敏感性影响不大,但β－胡萝卜素在加入ＤＰＱ 之后可以被光照破坏,这个过程可能与β－胡萝卜素的生理功能相关。     

巴氏碳球C_(60)对体外培养HeLa细胞的光敏杀伤效应

采用MTT比色分析法,观察了不同C_(60)浓度和不同光照强度下C_(60)对体外培养的HeLa细胞的光敏杀伤效应。结果表明,C_(60)在30μg/ml,光强4000Lux的条件下即可杀伤大部分细胞。受伤细胞圆缩、脱壁,里面颗粒增多,失去表面微绒毛状结构。当光强增大时,细胞表面甚至出现破损。     

Sun protection and Vitamin D: three dimensions of obfuscation

Ultraviolet (UV) radiation is a proven carcinogen, responsible for more than half of all human malignancies. It also compromises skin appearance and function. Since the UV action spectra for DNA damage, skin cancer and Vitamin D₃ (vit D) photosynthesis are identical and vit D is readily available from oral supplements, why has sun protection become controversial, now that some data suggest conventionally “sufficient” levels of vit D may be less than optimal for at least some population groups? First, the media and apparently some researchers are hungry for a new message. Nevertheless, after 50 years, UV exposure is still a major avoidable health hazard. Second, the controversy is fueled by a powerful special interest group: the indoor tanning industry. They target not the frail elderly or inner-city ethnic minorities, groups for whom evidence of vit D insufficiency is strongest, but rather fair-skinned teenagers and young adults, those at highest risk of UV photodamage. Third, evolution does not keep pace with civilization. When nature gave man the appealing capacity for vit D photosynthesis, the expected lifespan was far less than 40 years. Long-term photodamage was not a concern, and vit D was not available at the corner store. The medical community should avoid sensationalism and instead rigorously explore possible cause-and-effect relationships between vit D status and specific diseases while advocating the safest possible means of assuring vit D sufficiency.     

Environmental stress inhibits the synthesis de novo of proteins involved in the photodamage-repair cycle of Photosystem II in Synechocystis sp. PCC 6803

The Photosystem II complex (PSII) is susceptible to inactivation by strong light, and the inactivation caused by strong light is referred to as photoinactivation or photoinhibition. In photosynthetic organisms, photoinactivated PSII is rapidly repaired and the extent of photoinactivation reflects the balance between the light-induced damage (photodamage) to PSII and the repair of PSII. In this study, we examined these two processes separately and quantitatively under stress conditions in the cyanobacterium Synechocystis sp. PCC 6803. The rate of photodamage was proportional to light intensity over a range of light intensities from 0 to 2000 μE m⁻² s⁻¹, and this relationship was not affected by environmental factors, such as salt stress, oxidative stress due to H₂O₂, and low temperature. The rate of repair also depended on light intensity. It was high under weak light and reached a maximum of 0.1 min⁻¹ at 300 μE m⁻² s⁻¹. By contrast to the rate of photodamage, the rate of repair was significantly reduced by the above-mentioned environmental factors. Pulse-labeling experiments with radiolabeled methionine revealed that these environmental factors inhibited the synthesis de novo of proteins. Such proteins included the D1 protein which plays an important role in the photodamage-repair cycle. These observations suggest that the repair of PSII under environmental stress might be the critical step that determines the outcome of the photodamage-repair cycle.     

Comparative study of spectral and antioxidant properties of pigments from the eyes of two Mysis relicta (Crustacea, Mysidacea) populations, with different light damage resistance

Retinal visual and screening pigments of two populations (one marine and the other freshwater) of the opossum shrimp Mysis relicta Lovén (Crustacea, Mysidacea), which have different ocular tolerance to light, was investigated. Visual pigments were extracted by detergent and their bleaching difference spectra were determined. The difference between the visual pigment absorption maximum of the two populations correlated with their difference in spectral sensitivity. Using buffer or neutral methanol, a yellow pigment was extracted which had absorption maxima at 440 nm and 325 nm and bright blue fluorescence (λ_max 415 nm). A screening pigment (ommochrome) with maximum at 525 nm was extracted by acid methanol, and was probably related to the group of ommines. The eyes of the lake population had 1.8–2.7 times less of this pigment than the eyes of the sea population. The sea population is more resistant to photo-induced accumulation of thiobarbituric acid-reactive substances in eye tissues. This resistance may be due to the higher ommochrome content. Accepted: 8 December 1998     

Fluorescence Decaying Kinetics and Photodamage of Quinone-Reconstituted D1/D2/Cytochrome b559 Complex

Photosystem Ⅱ reaction center D1/D2/Cytochrome b559 complex loses its bound secondary electron acceptor QA and QB during isolation and purification. The artificial plastoquinone can reconstitute with the complex. The reconstitution of decyl-plastoquinone (DPQ) with D1/D2/Cytochrome b559 complex results in a decrease of the fraction of the two long lived fluorescence decay components (24 ns and 73 ns) coupled with photochemical activities to the total fluorescence yields, as well as a decrease of the total fluorescence intensity and a blue-shift of maximum emission wavelength. These results suggest that as the electron acceptor of reduced Pheo, DPQ restricts the charge recombination of P680+ Pheo-, and the two long lived fluorescence decay components (24 ns and 73 ns) come from the recombination. Although DPQ reconstitution has little effect on the susceptibility of Chi a to photodamage, β-carotene can easily be photodamaged after DPQ reconstitution. This is probably related to the physiological function of β-carotene.     

光系统Ⅱ反应中心D_1-D_2-Cyt b_(559)的光破坏作用研究

从高等植物叶绿体中分离得到的光系统Ⅱ(PSⅡ)反应中心D_1-D_2-Cytb(559)复合物很不稳定,极易受到光照的破坏。光照导致D_1-D_2-Cytb_(559)在红区(Qy带)的吸收光谱发生很大的变化,在最初光照45秒时间内,吸光度值升高,继续光照则吸光度值下降,而且680nm处的下降速度最大,吸收峰发生兰移,光照也导致荧光强度增大,发射峰兰移。所有这些结果表明,光破坏至少存在两个不同的过程,而且主要受到破坏的是原初电子供体P680。     

竹红菌甲素对红细胞膜的光损伤

光敏化剂竹红菌甲素在可见光区有三个吸收峰,其波长为475nm、545nm和585nm。在有竹红菌甲素存在时,红细胞膜样品用250W碘钨灯照射,其光强度为48尔格/平方毫米·秒。辐照后观察到以下一些效应:1)膜蛋白SH基含量减少。2)膜蛋白敏感的氨基酸残基,如组氨酸、半胱氨酸和色氨酸含量降低。3)膜蛋白发生光??聚集作用。4)多聚不饱和类脂发生过氧化作用。竹红菌甲素光照不同时间后和竹红菌甲素光照后放置一段时间,再加到红细胞膜中,均能观察到膜蛋白SH基含量降低。提示竹红菌甲素的光氧化产物是稳定的,能引起红细胞膜的光损伤。     

竹红菌甲素对红细胞膜和几种磷脂脂质体膜的流动性的光敏损伤

本文以荧光探针为手段,通过测量膜偏振度的变化,探讨了竹红菌甲素光敏作用对红细胞膜和几种磷脂脂质体膜的流动性的损伤。结果表明,甲素光敏作用使不同种类的磷脂(DPPC,DPPC/DPPE,红细胞膜磷脂)脂质体的流动性增加,其对光敏作用的敏感程度为红细胞膜磷脂脂质体显著小于DPPC/DPPE脂质体及DPPC脂质体。对红细胞膜来说,甲素光敏作用使其流动性呈现先降低而后增加的现象。去除膜上的spectrin以及用胰蛋白酶处理可使这种流动性变化的幅度受到抑制。据此,我们认为,膜磷脂,膜蛋白对甲素光敏作用中膜流动性的变化有着不同的影响,膜蛋白,特别是spectrin,是其中极重要的因素。     

干旱胁迫下大豆与玉米叶片光破坏的防御

随干旱强度的增加,大豆叶片光呼吸速率（Pr）降低的幅度小于Pn,使Pr／Pn比率升高。在轻度及中度干旱下,PSII光化学效率（Fv／Fm）能在暗置后较快地恢复。随干旱强度的增加,叶片光化学猝灭系数下降,非光化学猝死系数升高。干旱使叶片β－胡萝卜素及紫黄质含量下降,而玉米黄质含量（Z）与叶黄素库增加。与大豆相比,玉米在干旱条件下具有较高的Z含量和较大的叶黄素库。