Flavonoids are nearly ubiquitous in plants and are recognized as the pigments responsible for the colors of leaves, especially in autumn. They are rich in seeds, citrus fruits, olive oil, tea, and red wine. They are low molecular weight compounds composed of a three-ring structure with various substitutions. This basic structure is shared by tocopherols (vitamin E). Flavonoids can be subdivided according to the presence of an oxy group at position 4, a double bond between carbon atoms 2 and 3, or a hydroxyl group in position 3 of the C (middle) ring. These characteristics appear to also be required for best activity, especially antioxidant and antiproliferative, in the systems studied. The particular hydroxylation pattern of the B ring of the flavonoles increases their activities, especially in inhibition of mast cell secretion. Certain plants and spices containing flavonoids have been used for thousands of years in traditional Eastern medicine. In spite of the voluminous literature available, however, Western medicine has not yet used flavonoids therapeutically, even though their safety record is exceptional. Suggestions are made where such possibilities may be worth pursuing.

The Effects of Plant Flavonoids on Mammalian Cells:Implications for Inflammation, Heart Disease, and Cancer

There is a dynamic interplay between pro- and anti-oxidant substances in human ejaculate. Excessive reactive oxygen species (ROS) generation can overwhelm protective mechanism and initiate changes in lipid and/or protein layers of sperm plasma membranes. Additionally, changes in DNA can be induced. The essential steps of lipid peroxidation have been listed as well as antioxidant substances of semen. A variety of detection techniques of lipid peroxidation have been summarized together with the lipid components of sperm membranes that can be subjected to stress. It is unsolved, a threshold for ROS levels that may induce functional sperm ability or may lead to male infertility.

/pdf/reactive-oxygen-species-and-sperm-cells-4mc3jd3ayb.pdf

Reactive oxygen species and sperm cells.

This article consists of two parts: a brief overview of the ways in which free radicals can be involved in chemical carcinogenesis, and a review of cigarette smoke chemistry. Carcinogenesis is generally agreed to involve at least three stages: initiation, promotion, and progression. It is suggested that radicals sometimes are involved in the initiation step, either in the oxidative activation of a procarcinogen (such as benzo[a]pyrene) to its carcinogenic form or in the binding of the carcinogenic species to DNA, or both. The fraction of initiation events that involve radicals, as opposed to two-electron steps, is not known, but radicals probably are involved in a substantial number, although probably not a majority, of cancer initiation reactions. Promotion always involves radicals, at least to some extent. Progression probably does not normally involve radicals. The second part of this article reviews the molecular mechanisms involved in cigarette-induced tumors, particularly by aqueous cigarette tar (ACT) extracts and by a model of these solutions, aged solutions of catechol. ACT solutions as well as aged solutions of catechol contain a quinone-hydroquinone-semiquinone system that can reduce oxygen to produce superoxide and hence hydrogen peroxide and the hydroxyl radical. Both the cigarette tar radical and the catechol-derived radical can penetrate viable cells, bind to DNA, and cause nicks.

Cigarette smoke radicals and the role of free radicals in chemical carcinogenicity.

Background and Purpose—Several studies have implied an association between Chlamydia pneumoniae and atherosclerosis. Our research was designed to investigate the association of this organism with s...

Chlamydia pneumoniae Antibody Titers Are Significantly Associated With Acute Stroke and Transient Cerebral Ischemia The West Birmingham Stroke Project

Introduction The human inflammatory periodontal diseases are amongst the most common of chronic diseases to affect adults. In the UK, 69% of adults have early signs of disease and only 5% are completely free from clinical signs of inflammation.' The periodontal complex comprises alveolar bone, periodontal ligament, root cementum, and the overlying gingival (gum) tissues (fig 1). Gingivitis may be defined as "an inflammatory lesion, mediated by hostparasite interactions, that is confined to the gingival tissues". The major cause of gingivitis is an accumulation of microbial plaque in and around the dento-gingival complex, which, when removed, results in complete resolution of the inflammatory lesion.2 Periodontitis is regarded as "an inflammatory lesion, mediated by complex host-parasite interactions, that leads to the loss of connective tissue attachment to root surface cementum and adjacent alveolar bone". There are many forms of periodontitis' and the changes associated with periodontitis are irreversible, resulting in tooth loss and substantial morbidity in medically compromised patients, where a focus of infection and subsequent bacteraemia may present a major risk. The mouth possesses a unique hard/soft tissue barrier, that separates the internal systems from the external environment. The barrier (fig 1) is called the junctional epithelium and is permeable to external (bacterial) material passing into the adjacent connective tissues and blood stream, and to products of internal defence systems (leucocytes, complement, antibodies, pro-inflammatory cytokines, etc.) passing outwards. To assist this vulnerable barrier in protecting the underlying host tissues from damage by products of bacterial plaque, a fluid, gingival crevicular fluid (GCF), is produced from beneath the gingival margin. In health, GCF is a serum transudate containingall components of serum and also polymorphonuclear leucocyte cells, but during disease many products of the host-parasite conflict enter the fluid, which becomes a true exudate. GCF may be collected non-invasively on paper strips4 (fig 2), providing an ideal medium in which to study the complex bacterial-host interactions (fig 3) that characterise other similar inflammatory disorders. Substantial data are available in the literature on the role of reactive oxygen species (ROS) and antioxidants in disorders such as the inflammatory lung diseases and in chronic immune mediated conditions such as rheumatoid arthritis. However, remarkably little information is available on the periodontal diseases, which show many of the pathological features of other chronic inflammatory diseases. The periodontal tissues also provide an ideal medium within which to study mechanisms of ROS mediated tissue damage and of antioxidant defence in response to bacterial colonisation, through the non-invasive collection of GCF. This paper, therefore, attempts to review current knowledge of free radical damage and antioxidant defence systems in inflammatory diseases, and to use the inflammatory periodontal diseases as a focus for discussion. Emphasis is placed upon the presence of low molecular weight thiols such as reduced glutathione (GSH) and cysteine in fluids that bathe vulnerable epithelial surfaces, and it is postulated that new therapeutic pathways may be found by using cysteine and GSH preserving drugs-for example, N-acetylcysteine, or indeed, inhibitors of the nuclear transcription factor NF-KB.

https://mp.bmj.com/content/molpath/49/5/M247.full.pdf

H Esterbauer

Papers

Hydroalkenals: cytotoxic products of lipid peroxidation