Ferroptosis as a mechanism of non-ferrous metal toxicity.

Ferroptosis is a recently discovered form of regulated cell death, implicated in multiple pathologies. Given that the toxicity elicited by some metals is linked to alterations in iron metabolism and induction of oxidative stress and lipid peroxidation, ferroptosis might be involved in such toxicity. Although direct evidence is insufficient, certain pioneering studies have demonstrated a crosstalk between metal toxicity and ferroptosis.

Isolevuglandins (isoLGs) as toxic lipid peroxidation byproducts and their pathogenetic role in human diseases.

Lipid peroxidation results in generation of a variety of lipid hydroperoxides and other highly reactive species that covalently modify proteins, nucleic acids, and other lipids, thus resulting in lipotoxicity. Although biological relevance of 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA) is well studied, the existing data on the role of isolevuglandins (isoLGs) in pathology are insufficient. Therefore, the objective of the present study was to review the existing data on biological effects of isoLG and isoLG adducts and their role in multiple diseases.

Effect of Zn Supplementation on Trace Element Status in Rats with Diet-Induced Non-alcoholic Fatty Liver Disease.

The present study aimed to assess the effect of Zn supplementation on trace element levels in the liver, serum, and hair of rats with dietary-induced non-alcoholic fatty liver disease (NAFLD). A total of 26 3-month-old female Wistar rats were divided into four groups: control, NAFLD, Zn-supplemented (227 mg/L zinc as Zn sulfate Zn(SO) dissolved in a drinking water), and NAFLD-Zn-supplemented. NAFLD was verified by histological assessment of liver samples.

Pleiotropic functions of plasmacytoid dendritic cells in the pathogenesis of the rheumatoid arthritis.

Rheumatoid arthritis is a chronic autoimmune inflammatory disease with an unclear etiology. The disease is characterized by infiltration of synovial tissue with immune cells, among which there are dendritic cells that play multifaceted roles in the pathogenesis of the disease. Here we shall assume that plasmacytoid dendritic cells are able to change their phenotype under the influence of various stimuli, thereby modulating the course of the disease, contributing to both the development of exacerbations and the induction of remissions depending on the phenotype they have acquired.

Alteration of local adipose tissue trace element homeostasis as a possible mechanism of obesity-related insulin resistance.

The mechanisms of association between obesity and the related metabolic disturbances in general and insulin resistance in particular are extensively studied. Taking into account a key role of adipose tissue insulin resistance in the development of systemic obesity-related insulin resistance, the estimation of mechanisms linking increased adiposity and impaired insulin signaling in adipocytes will allow to develop novel prophylactic and therapeutic approaches to treatment of these states. A number of trace elements like chromium, zinc, and vanadium have been shown to take part in insulin signaling via various mechanisms.

Mercury and metabolic syndrome: a review of experimental and clinical observations.

A significant interrelation between heavy metal exposure and metabolic syndrome (MetS) development has been demonstrated earlier. Despite the presence of a number of works aimed at the investigation of the role of Hg in MetS development, the existing data remain contradictory. Therefore, the primary objective of the current work is to review the existing data regarding the influence of mercury on universal mechanisms involved in the pathogenesis of the development of MetS and its components.