Oxidative stress is a state of imbalance between the process of producing and removing reactive oxygen species (ROS). With advancing age or in certain situations where oxidative stress cannot be combated, various pathologies such as inflammatory bowel diseases or neoplasia may occur. Over the past decade, a surge of intriguing discoveries has linked subtoxic levels of oxidative stress to key processes, including the maintenance of mucosal homeostasis, regulation of protective inflammation, and even the control of tissue wound healing. Given the complexity and limited understanding of oxidative mechanisms involved in human intestinal pathology, the relevance of experimental models becomes a critical consideration in efforts to elucidate these processes. Although diverse, none of these models fully replicate human digestive pathology; however, they remain valuable for developing new therapeutic strategies. This paper examines the main markers of oxidative stress and its mechanism and their impact on the intestinal tract, as well as the most widely used animal models that have contributed valuable insights into the pathogenesis of inflammatory bowel diseases (IBD).

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease with progressive evolution and high mortality. Magnesium, copper and zinc are essential biometals involved in numerous biological processes in all organs of the human body. A lower level of zinc and magnesium and a higher cooper/zinc ratio are frequently encountered in patients with idiopathic pulmonary fibrosis but also in other forms of pulmonary fibrosis. These imbalances are involved in the main pathogenic mechanisms of idiopathic pulmonary fibrosis: alveolar epithelial cell lesions, oxidative stress, inflammation, fibroblast and myofibroblast proliferation, mitochondrial activity, excessive extracellular matrix accumulation, high collagen production, alveolar macrophage dysfunctions, and apoptosis. A multitude of experimental and clinical studies have shown the importance of these bivalent cations for the synthesis or activity of some important endogenous active substances (fatty acids, eicosanoids, sirtuin1, p53 protein, interleukins, growth factors, some enzymes, and others) involved in one form or another in the pathogenesis of IPF. There are no randomized clinical trials yet, but some clinical and experimental results suggest that the association of zinc and magnesium with pirfenidone and nintedanib could be beneficial and should be assessed as soon as possible after the onset of this disease. The correction of hypomagnesemia and hypozincemia, whenever they exist, must be performed as soon as possible after the diagnosis of fibrosis.