Disease relevance of ROSE BENGAL

• In a study of aerobically perfused rat hearts, the in situ photoactivation (530-590 nm) of rose bengal (a process that leads to the production of singlet oxygen and superoxide) has been shown to lead to the rapid development of electrocardiographic abnormalities and arrhythmias [1].
• Photodynamic inactivation of infectivity of human immunodeficiency virus and other enveloped viruses using hypericin and rose bengal: inhibition of fusion and syncytia formation [2].
• Rapid electrophysiological changes leading to arrhythmias in the aerobic rat heart. Photosensitization studies with rose bengal-derived reactive oxygen intermediates [3].
• Then, regional ischemia was induced, and rose bengal-free perfusion was restored [4].
• An intravenous infusion of a photosensitising dye, rose bengal (20 mg/kg body weight), was administered over 90 seconds, beginning at the start of irradiation [5].

Psychiatry related information on ROSE BENGAL

• Published methods for radioiodination of rose bengal require reaction times of 1 hr or more at temperature from 50 to 120 degrees C. Through the use of an acidified ethanol solvent and potassium iodate oxidant, purified rose bengal is radioiodinated at room temperature within 15 min with chemical yields ranging between 93 and 97% [6].

High impact information on ROSE BENGAL

• Induction of thyroid tumors in (C57BL/6N x C3H/N)F1 mice by oral administration of 9-3',4',5',6'-tetrachloro-o-carboxy phenyl-6-hydroxy-2,4,5,7-tetraiodo-3-isoxanthone sodium (Food Red 105, rose bengal B) [7].
• The tumorigenicity of 9-3',4',5',6'-tetrachloro-o-carboxy phenyl-6-hydroxy-2,4,5,7-tetraiodo-3-isoxanthone sodium (CAS: 632-68-8) [also called Food Red 105 (FR 105) or Rose Bengal B], which is widely used for food or cosmetic coloring in Japan, was examined in (C57BL/6N X C3H/N)F1 mice [7].
• Albumin-mediated transport of rose bengal by perfused rat liver. Kinetics of the reaction at the cell surface [8].
• These observations were supported by in vitro electrochemical measurements that revealed the following order with respect to ease of reduction: cercosporin >> eosin Y > rose bengal [9].
• Singlet oxygen-induced arrhythmias. Dose- and light-response studies for photoactivation of rose bengal in the rat heart [1].

Chemical compound and disease context of ROSE BENGAL

• METHODS: Rats were anesthetized with halothane and preloaded with 111In-tropolone-labeled platelets (50 to 80 microCi) 30 minutes before nonocclusive common carotid artery thrombosis induced by a rose bengal-mediated photochemical insult [10].
• Four photosensitizers (methylene blue (MB), rose bengal (RB), uroporphyrin (UP) and aluminum phthalocynine tetrasulphonate (AIPcS4)) could inactivate the adenovirus, as measured by expression of the luciferase reporter gene and by plaque assay [11].
• METHODS: Animals were bilaterally infected with HSV-1 strain H129, and at daily intervals up to 16 days post infection (dpi) rose bengal or lissamine green B was instilled in the left eyes [12].
• The effect of induced hypothyroidism (by feeding an antithyroid drug-propylthiouracil) on the transport and clearance of the routinely used hepatobiliary radiopharmaceuticals--radioiodinated iodine-131 (131I) rose bengal and technetium-99m-N-(4-n-butylphenylcarbamoylmethyl) iminodiacetate, was studied in the rats [13].
• Fluorescein differs from rose bengal in its lack of intrinsic toxicity, photodynamic action, and ability to be blocked by the above-mentioned substances [14].

Biological context of ROSE BENGAL

• Photoactivation of rose bengal had no effect on heart rate but caused a transient (0-4 minutes) vasodilation followed by a progressive vasoconstriction [1].
• Rat hearts (n = 6 per group) were perfused aerobically at 37 degrees C for 10 minutes without rose bengal and for 5 minutes with rose bengal (250 nmol/l), during which time no changes in coronary flow or heart rate were observed [3].
• Single ventricular cells exposed to rose bengal (10-100 nM) exhibited spontaneous membrane potential fluctuations at plateau potentials and at the level of the resting membrane potential [15].
• We reported previously that singlet oxygen, generated by irradiation of rose bengal with visible light, induced apoptosis in human promyelocytic leukemia HL-60 cells [16].
• Progress of lipid peroxidation, induced by aerobic photoexcitation of rose bengal, was monitored by the detection of lipid hydroperoxides and by electron spin resonance oximetry [17].

Anatomical context of ROSE BENGAL

• We investigated the role of singlet oxygen (generated from photoactivation of rose bengal) on the calcium transport and Ca(2+)-ATPase activity of cardiac sarcoplasmic reticulum (SR) [18].
• Here we show the in vitro photodynamic effect of rose bengal activated by intracellular generation of light, in luciferase-transfected NIH 3T3 murine fibroblasts [19].
• Firefly luciferin-activated rose bengal: in vitro photodynamic therapy by intracellular chemiluminescence in transgenic NIH 3T3 cells [19].
• Photoillumination (wave length, 540 nm) was applied to the middle cerebral artery, and then rose bengal (20 mg/kg) was administered intravenously [20].
• Multiple cerebral arterioles were occluded by platelet aggregates containing frequent erythrocytes and leukocytes, identical to the thrombotic material in the carotid artery but different from the platelet aggregates seen in the carotid artery and the brain in the rose bengal model [21].

Associations of ROSE BENGAL with other chemical compounds

• 1O2 was produced in photosensitizing systems using rose bengal or methylene blue as sensitizers and was detected as TEMP-1O2 product (TEMPO) by electron paramagnetic resonance (EPR) spectroscopic techniques [22].
• Interestingly, pre-treatment of plants with the radical-scavenging compound N-acetyl-l-cysteine (NAC) led to a significantly lower recombination increase upon grafting after treatment with UVC and RB [23].
• In Model I, the right middle cerebral artery (MCA) was exposed via a subtemporal craniotomy in halothane- and nitrous oxide-anesthetized Wistar rats and was occluded photochemically by irradiation with an argon ion laser following the intravenous administration of the photosensitizing dye rose bengal [24].
• Six [203Hg] hydroxymercurifluoresceins were prepared by two methods and compared with [3H] fluorescein, [131I] rose bengal, and [203Hg] mercuric nitrate, in a rat model for myocardial necrosis, to determine their specificities for damaged myocardium (DM) [25].
• Sulfobromophthalein (BSP), bromophenol blue (BPB) and rose bengal (RB) induced a transient increase in the plasma concentration of ANS (the so-called 'counter-transport' phenomena) [26].

Gene context of ROSE BENGAL

• RESULTS: The cytoplasm and nucleus of confluent HCLE cells cultured in media without serum, lacking the expression of MUC16 but not MUC1, as well as human corneal fibroblasts, which do not express mucins, stained with rose bengal [27].
• The activation of ERK 1/2 and Akt as induced by stimulation with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF) was inhibited by 1O2 generated intracellularly upon photoexcitation of rose Bengal (RB) [28].
• In contrast, extracellular generation of 1O2, by irradiation of Rose Bengal immobilized on agarose beads or by chemiexcitation employing the hydrophilic 1,4-endoperoxide of disodium 3,3'-(1,4-naphthylidene) dipropionate, was ineffective in activating p38 or JNK [29].
• Mucin characteristics of human corneal-limbal epithelial cells that exclude the rose bengal anionic dye [27].
• The expression of a Yap1p-dependent reporter gene was induced by increased singlet oxygen production, showing that singlet oxygen activates general oxidative stress response mechanisms required for the resistance against Rose Bengal treatment [30].

Analytical, diagnostic and therapeutic context of ROSE BENGAL

• To assess the reversibility of rose bengal-induced effects, hearts (n = 6/group) were perfused with rose bengal (250 nmol/l) for 1, 2, 4, 6, and 20 minutes followed by perfusion in the dark for 19, 18, 16, 14, and 0 minutes, respectively [1].
• Additional studies revealed that rose bengal photoactivation without reperfusion was less arrhythmogenic compared with the combination of reperfusion plus photoactivation [4].
• The results were also confirmed by high-performance liquid chromatography of the SR exposed to irradiated rose bengal [18].
• After the intravenous injection of rose bengal, a potent photosensitizing dye, an ischemic lesion was formed by irradiating the left parietal convexity of the exposed skull for 20 minutes with green light (560 nm) from a filtered xenon arc lamp [31].
• Fluorescence titrations with ANS and rose bengal yielded affinity constants of 3.9 X 10(3) and 6 X 10(5) M-1, respectively [32].

References