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Aim: The objective of the study was to look the efficacy of fractionated light against Streptococcus mutans biofilm., Materials & Methods: Antibiofilm assays (crystal violet, congo red), electron microscopic, confocal and spectroscopic studies were performed to check the effect of fractionated light., Results: 6-6.5 log 10 reduction of planktonic and 3.6-4.2 log 10 reduction in biofilm were observed after irradiation with fractionated as compared with continuous light. Increased permeability to propidium iodide and leakage of cellular constituent validate the greater antibiofilm effect of fractionated light. Spectroscopic studies confirmed the relative contribution of type I and type II photochemistry., Conclusion: Phenothiazinium dyes have a potential against bacterial biofilm in combination with light fractionation and it offers new opportunities to explore its clinical implication.

Through dental procedures and environment, periodontal tissues are exposed to many types of reactive oxygen species (ROS). Recently, various forms of antioxidants have been introduced as an approach to fight dental diseases and improve general gingival health. This article focuses on the classification of antioxidants and the link between oxidative stress and periodontal disease. The protective mechanisms of antioxidants and how routine dental procedures may increase ROS is discussed. The final section reviews the effect of tobacco products on gingival health and disease.

Reactive oxygen species have been implicated in the pathogenesis of virtually every stage of vascular lesion formation, hypertension, and other vascular diseases. We are currently gaining insight into important sources of reactive oxygen species in the vessel wall, including the NADPH oxidases, xanthine oxidase, uncoupled nitric oxide synthase, and mitochondrial sources. Although various reactive oxygen species have pathological roles, some serve as important signaling molecules that modulate vascular tone, growth, and remodeling. In the next several months, a series of articles in Arteriosclerosis, Thrombosis, and Vascular Biology attempt to further elucidate how reactive oxygen species are produced by vascular cells and the roles of these in vascular homeostasis. This series promises to provide a valuable update on a wide variety of issues related to the biochemistry, molecular biology, and physiology of these important and fascinating molecules. Reactive oxygen species have been implicated in the pathogenesis of virtually every stage of vascular lesion formation, hypertension, and other vascular diseases. Upcoming series of articles in Arteriosclerosis, Thrombosis, and Vascular Biology help elucidate how reactive oxygen species are produced by vascular cells and their role in vascular homeostasis.

A great number of drugs, toxicants, and growth factors induce the generation of intermediary reactive oxygen species (ROS). The human promyelocytic leukemia HL60 cell line differentiated along the macrophage or neutrophil lineage is a model system that is frequently used for the generation of ROS by various agents. As a primary source of ROS the superoxide anion produced by an enzymatic complex, NADPH oxidase, is well established. The present study shows that nondifferentiated HL60 cells contain NADPH oxidase and can be used as a model for the assessment of oxidant as well as antioxidant compounds. The expression of the multicomponent NADPH oxidase was demonstrated in nondifferentiated HL60 cells at the molecular level by detection of the mRNAs of the components gp91phox, p47phox, and p67phox as well as functionally by phorbol 12-myristate-13-acetate (PMA)-stimulated generation of superoxide, which was susceptible to inhibition by diphenyleneiodonium. The functional assay was performed using the cells in a log growth phase by adapting a standard microplate assay based on the classic superoxide dismutase-inhibitable reduction of cytochrome c. Validation of the microplate assay was carried out both with nonadherent differentiated HL60 cells and the adherent mouse monocyte-macrophage-like RAW 264.7 cell line, as well as with various compounds of oxidant (bleomycin sulfate, cis-diammineplatinum(II), camptothecin, TNF-alpha, IL-1 beta), nonoxidant (4 alpha-PMA, piracetam), and antioxidant (alpha-tocopherol, ascorbic acid) activity. In summary, we established a highly specific, reproducible and--with the aid of the nondifferentiated HL60 cell line--time-saving superoxide microplate assay as a valuable tool for the rapid screening of compounds for oxidative and antioxidative activity.

Reactive oxygen species (ROS) are generated when oxygen is supplied in excess and/or its reduction is insufficient. The best explored ROS are superoxide anions, hydroxyl radicals and hydrogen peroxide. The first two are free radicals. ROS are harmful for the living cells and are implicated in a variety of pathological processes and diseases. Drugs used in the treatment of these states are either stimulators of endogenous defense mechanisms against ROS or inhibitors of ROS formation. Six groups of anti-ROS substances have been described in this paper. 1) Antioxidant substances used in substitutive therapy such as enzymes (e.g. superoxide dismutase), substances containing thiol groups and vitamins (A, E, P, C). 2) Chelating agents (e.g. desferoxamine), which lower the level of prooxidative transition metal ions. 3) Inhibitors of superoxide ions generation by stimulated cells or xanthine oxidase. Such mechanism of action was described for xanthine oxidase inhibitor-allopurinol. 4) Superoxide scavengers. Many known drugs were investigated for this activity, but the best documentation was presented for flavonoids. 5) Substances which eliminate hydrogen peroxide, mainly glutathione and its precursors. 6) Scavengers of hydroxyl radicals. Studies of the above activity were conducted mainly using an unspecific method--estimation of malondialdehyde generated during the action of hydroxyl radicals on lipids or on desoxyribose. Inhibition of malondialdehyde formation was described for many drugs of plant and synthetic origin.