Ischemia and reperfusion (I/R) causes a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to the ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, and inflammatory responses to cell death. In normal conditions, ROS mediate important beneficial responses. When their production is prolonged or elevated, harmful events are observed with peculiar cellular changes. In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. The mechanisms underlying the activation of NLRP3 are several and not completely elucidated. It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation. Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated.

Progression of the HeLa cell through its life cycle is accompanied by centriolar replication and pericentriolar changes that are in synchrony with DNA synthesis and mitosis. The first signs of preparation for replication occur during G1 at which time the two orthogonal centrioles separate. Replication by budding begins at/or near the initiation of DNA synthesis and is completed by G2. Pericentriolar changes which probably are causally related to spindle tubule formation occur at this time and include the appearance of vesicles, electron-opaque bodies, and an amorphous pericentriolar halo. These phenomena begin to disappear by late prophase, and the remainder of mitosis manifests decreasing centriolar and pericentriolar activity.

Background: Cadmium (Cd) is a heavy metal particularly hazardous for human health, as it is highly diffused and, therefore, a ubiquitous environmental toxicant. In fact, in the general population, the main sources of exposure are food, cigarette smoking, inhalation of ambient air, drinking water, contaminated soil or dust. Furthermore, an occupational exposure usually involves human during mining, fume inhalation or manufacturing nickel-cadmium battery, electroplating and paint pigments that utilize Cd. Methods: We undertook a structured search in literature about Cd. This metal is noxious on the cells of many organs, among which the kidney, the testis and the brain will be considered in this review. Results: The toxic effects induced by Cd include many specific mechanisms, such as the oxidative stress, cellular death and inflammation. As no specific therapy for the prevention or treatment of the morbidity and mortality associated with Cd exposure is available, the state of the art of the therapeutic approaches is illustrated. Conclusion: Nowadays, a therapy able to counteract Cd toxicity is still lacking and the development of new therapeutic agents is requested.

Objective: Broad antiinflammatory effects following adenosine A_2A receptor stimulation have been demonstrated in acute inflammatory diseases, including arthritis. Polydeoxyribonucleotide (PDRN) activates the adenosine A_2A receptor. This study was undertaken to investigate the effects of PDRN in collagen‐induced arthritis (CIA) in mice.Methods: Arthritis was induced in DBA/1 mice by an intradermal injection of 100 μl of bovine type II collagen in Freund's complete adjuvant. Mice were immunized a second time 21 days later. Control animals received 100 μl of a saline solution. Animals with CIA were randomized to receive one of the following: vehicle (1 ml/kg); PDRN (8 mg/kg intraperitoneally daily); 3,7‐dimethyl‐propargylxanthine (DMPX), a specific adenosine A_2A receptor antagonist (0.1 mg/kg intraperitoneally daily); or PDRN plus DMPX. The treatment was initiated immediately after the second immunization and continued to day 45. Clinical evaluation of arthritis was performed throughout the study. On day 45, the animals were killed and the severity of arthritis was evaluated histologically. Cartilage expression and circulating levels of high mobility group box chromosomal protein 1 (HMGB‐1), tumor necrosis factor α (TNFα), interleukin‐6 (IL‐6), and IL‐10 were investigated. Inflammatory cytokine production was also evaluated in stimulated human chondrocytes treated with PDRN.Results: PDRN treatment significantly ameliorated clinical signs of arthritis, improved histologic damage, reduced the cartilage expression and circulating levels of HMGB‐1, TNFα, and IL‐6, and enhanced IL‐10 expression. The concomitant administration of DMPX and PDRN ablated the PDRN‐induced protective effect in experimental arthritis. PDRN also reduced cytokine production from stimulated human chondrocytes.Conclusion: Our findings indicate that PDRN may represent a new alternative for the treatment of arthritis.