Excess Iodine Consumption Induces Oxidative Stress and Pancreatic Damage Independently of Chemical Form in Male Wistar Rats: Participation of PPAR-γ and C/EBP-β.

Background: Human beings consume different chemical forms of iodine in their diet. These are transported by different mechanisms in the cell. The forms of iodine can be part of thyroid hormones, bind to lipids, be an antioxidant, or be an oxidant, depending on their chemical form.

Iodine Promotes Glucose Uptake through Akt Phosphorylation and Glut-4 in Adipocytes, but Higher Doses Induce Cytotoxic Effects in Pancreatic Beta Cells.

Background: Epidemiological clinical reports have shown an association between iodine excess with diabetes mellitus type 2 and higher blood glucose. However, the relationship between iodine, the pancreas, adipose tissue, and glucose transport is unclear. The goal of this study was to analyze the effect of iodine concentrations (in Lugol solution) on glucose transport, insulin secretion, and its cytotoxic effects in mature 3T3-L1 adipocytes and pancreatic beta-TC-6 cells.

Iodine induces toxicity against and through oxidative stress.

Background And Objectives: Candida species are antifungal-resistant opportunistic infections that spread through contaminated medical staff hands and hospital surfaces creating a nosocomial infection risk. Iodine's antibacterial properties are well established; however, its antifungal properties remain unknown. The objective of this study was to investigate the antifungal effects of lugol on cell viability and oxidative stress on and strains

Materials And Methods: MTT reduction test and sensitivity growth assay were used to determine viability and minimal inhibitory concentration, colorimetric tests were used to analyzing lipoperoxidation and antioxidant status in , parental lacking catalase gene () and superoxide dismutase 1 and 2 double mutants (Δ Δ) strains exposure to lugol were used.