Endocrine-Independent Cytotoxicity of Bisphenol A Is Mediated by Increased Levels of Reactive Oxygen Species and Affects Cell Cycle Progression.

Bisphenol A (BPA) is used for the production of plastics and epoxy resins, which are part of packaging materials for food and beverages, and can migrate into food and the environment, thus exposing human beings to its effects. Exposure to BPA has been associated with oxidative stress, cell cycle changes, and genotoxicity, and is mediated by its known endocrine-disrupting activity. Possible BPA cytotoxicity without mediation by estrogen receptors has been reported in the literature. Here, we show the toxic effects of BPA by live-cell imaging on the fission yeast Schizosaccharomyces pombe, an experimental model lacking estrogen receptors, which were in line with data from flow cytometry on intracellular oxidation (76.4 ± 14.4 and 19.4 ± 16.1% of fluorescent cells for BPA treatment and control, respectively; p < 0.05) as well as delay in cell cycle progression (after 90 min of experiment, 48.4 ± 4.30 and 64.6 ± 5.46% of cells with a 4C DNA content for BPA treatment and control, respectively; p < 0.05) upon exposure to BPA. These results strongly support the possibilities that BPA-induced cell cycle changes can be independent of estrogen receptors and that live-cell imaging is a powerful tool for genotoxic analysis.

Bisphenol A as an environmental pollutant with dual genotoxic and DNA-protective effects.

OBJECTIVES: Bisphenol A (BPA) is an endocrine disruptor which has been shown to be a harmful compound for living organisms. It is the main component of the most commonly used plastic products such as plastic bottles, food cans and containers or dental fillings, and other medical aids. Recently, it has become a new environmental pollutant. The current knowledge about the BPA effects (including genotoxic one) on different cells is in many cases contradictory. Thus, the aim of the paper is to study the potential genotoxic effect of BPA. METHODS: An observation of the genotoxic activity of BPA on human lymphocytes was evaluated by using the alkaline comet assay and a modified comet assay with bacterial DNA repair enzyme Fpg. The potential DNA-protective effect of BPA was tested by using the DNA-topology assay. RESULTS: The results show that rising concentrations of BPA increase the risk of DNA double-strand breaks and modified purines in human lymphocytes. Interestingly, BPA shows an ability to protect plasmid DNA from the damage of iron ions in cell-free system. CONCLUSIONS: BPA itself does not induce genotoxic effect to DNA. However, BPA treatment of human lymphocytes leads to the induction of DNA damage. The proposed mechanism of BPA action in the human lymphocytes could be mediated by cell metabolism that induces an oxidative stress and ROS formation. ROS subsequently attack DNA and thus induce DNA damage. According to our results, BPA can be included in the group of substances with dual effects involving genotoxic and DNA-protective activity.

Mechanism of increased mortality in hemodialysed patients with periodontitis.

Periodontitis significantly decreases survival in hemodialysed patients with end stage renal disease (ESRD). Periodontitis-related microorganisms spreading into the bloodstream are thought to impair blood rheological parameters - for example, increasing whole blood viscosity, aggregating blood elements, and decreasing blood flow - and thereby significantly accelerate systemic or local diseases, impairing survival. We discuss the ability of a prototypical pathogenic anaerobic polybacterial consortium to modulate and interfere with host immune responses and to enzymatically degrade host proteins, to bind to and cleave extracellular matrix proteins, to invade intercellularly as well as intracellularly, to promote vascular permeability, to disrupt polymorphonuclear leukocyte function, to cleave complement, and to degrade IgG heavy chains. To further elucidate these phenomena, studies involving detecting microorganism byproducts and monitoring blood rheological parameters are necessary.

Mechanism of traumatic neuroma development.

We suggest that symptomatic traumatic neuromas - benign lesions of incompletely understood etiology - develop when neural fiber regeneration occurs in the presence of excessive fibrous tissue proliferation. Subsequent contraction of wound and scar myofibroblasts leads to compression of the regenerating nerve fibers and further stimulation of the overgrowth of their perineurial cells as a protective response. This chronic process leads to a slow enlargement of the proliferating mass and the typical histological picture of a traumatic neuroma, in which multiple interlacing fascicles of nerve fibers are encased in condensed fibrous tissue. To avoid the development of a traumatic neuroma, we propose that an injured or a transected nerve should be placed out of the site of potential excessive fibroproduction and/or that all external factors leading to excessive fibroproduction development be eliminated from the wound site.

Surgical treatment of primary hyperparathyroidism in children: report of 10 cases.

Primary hyperparathyroidism in children is very rare. It is caused by overproduction of parathormone by a pathologically changed parathyroid gland. We carried out a retrospective study in 10 patients (age 10-17 years) who had surgical treatment between 1996 and 2007. The main signs of primary hyperparathyroidism were urolithiasis, nephrolithiasis, nephrocalcinosis and bone resorption, as well as non-specific signs such as fatigue, torpidness and muscle weakness. Patients were examined using sonography, MIBI-scintigraphy, CT and MRI. Calcium was measured before and after surgery; parathormone was monitored postoperatively. Surgery was curative in nine patients; reoperation was necessary in one patient because an ectopic parathyroid gland was not detected during the primary operation. Other major complications were not observed. Removal of pathologically changed parathyroid glands offers definitive and safe treatment of primary hyperparathyroidism in children. Special care should be taken if an ectopic parathyroid gland is suspected.

Clinical implications of a close vicinity of nervus dorsalis penis/clitoridis and os pubis.

INTRODUCTION: Close relation of nervus dorsalis penis/clitoris and os pubis has a major impact in surgical disciplines. AIM: To summarize a current knowledge about this region, represented by the course of sulcus nervi dorsalis penis/clitoridis. METHODS: Literature search of years 1970-2007. MAIN OUTCOME MEASURES: In male, it accommodates nervus dorsalis penis whereas in female nervus et arteria dorsalis clitoridis. Lateral border of sulcus nervi dorsalis penis corresponds to vertical ridge and lateral border of sulcus nervi dorsalis clitoridis to ventral arc-two parameters, which are parts of the Phenice's method for sexing of isolated os pubis. RESULTS: Exact preparation of nervus dorsalis penis is crucial in correct performance of conversion of genitalia in patients with transsexualism, in reconstruction of posterior urethra, in hypospadia, during performance of penile blockade during circumcision and in revascularization surgery of erectile dysfunction. Possible role of the sulcus nervi dorsalis penis in the Alcock's syndrome is discussed. Similarly, it is advisable to take care of nervus dorsalis clitoridis during reduction clitoridoplasty in patients with adrenogenital syndrome and during the insertion of transobturator vaginal tape. Injury of nervus dorsalis penis/clitoridis leads to hypesthesia or anesthesia of glans penis/clitoridis. The injury to arteria dorsalis clitoridis leads to bleeding and/or hematoma. CONCLUSIONS: Clinical anatomy of sulci is important in several situations in urologic surgery. It is possible to use sulcus nervi dorsalis penis/clitoridis for sexing of isolated pubis for anthropological or forensic purposes.