Proper joint function has a significant impact on people’s quality of life. Joints are the point of connection between two or more bones and consist of at least three elements: joint surfaces, the joint capsule, and the joint cavity. Joint diseases are a serious social problem. Risk factors for the development of these diseases include overweight and obesity, gender, and intestinal microbiome disorders. Another factor that is considered to influence joint diseases is trace elements. Under normal conditions, elements such as iron (Fe), copper (Cu), cobalt (Co), iodine (I), manganese (Mn), zinc (Zn), silver (Ag), cadmium (Cd), mercury (Hg), lead (Pb), nickel (Ni) selenium (Se), boron (B), and silicon (Si) are part of enzymes involved in reactions that determine the proper functioning of cells, regulate redox metabolism, and determine the maturation of cells that build joint components. However, when the normal concentration of the above-mentioned elements is disturbed and toxic elements are present, dangerous joint diseases can develop. In this article, we focus on the role of trace elements in joint function. We describe the molecular mechanisms that explain their interaction with chondrocytes, osteocytes, osteoblasts, osteoclasts, and synoviocytes, as well as their proliferation, apoptosis, and extracellular matrix synthesis. We also focus on the role of these trace elements in the pathogenesis of joint diseases: rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and systemic lupus erythematosus (SLE). We describe the roles of increased or decreased concentrations of individual elements in the pathogenesis and development of joint diseases and their impact on inflammation and disease progression, referring to molecular mechanisms. We also discuss their potential application in the treatment of joint diseases.

Background: Multiple myeloma (MM) is a hematologic malignancy, which causes accumulation of plasma cells in the bone marrow. The symptoms of MM are associated with organ dysfunction and include hypercalcemia, renal failure, anaemia and bone destruction. A relatively new and promising therapeutic option for MM is CAR-T therapy. Aim of the study: The study aimed to outline the role of CAR-T therapy in MM treatment.Material and methods: We conducted a literature review containing 24 articles. We described the role of CAR-T in MM therapy, its therapeutic points, the effectiveness of therapy, and its side effects.Results: CAR-T cells transduced with CAR can recognize specific antigens and kill the cancer cells. For MM these specific antigens are integrin β7, SLAMF7, CD138, BCMA, GPRC5D and FCRL5. Integrin β7 in its active form, can be found in MM cells, whereas in other blood cells, integrin β7 is in the inactive form. The expression of SLAMF7 on MM cells is high and uniform, but its function is not clear: expression of SLAMF7 in MM is suspected to increase the survival and adhesion of MM cells to bone marrow stromal cells. CD138's strong expression on MM cells is contributing to their development and proliferation. BCMA expression was not detected in other human tissues, only in MM cells. GPRC5D is highly expressed in bone marrow samples from MM patients, and minimally expressed in other hematologic malignancies. FCRL5 is a protein marker found specifically on plasma cells in MM, its increased expression promotes B cell proliferation. The AlloCAR-T therapy also seems to be an effective method.CAR-T therapy has also adverse effects including cytokine release syndrome, neurological toxicity, haematological disorders and infusion fever. Conclusions: The effects of CAR-T therapy in MM are really promising and give real benefits to patients. For this reason, it should be further developed and subjected to further research.

The female reproductive system, particularly the ovary, exhibits a high sensitivity to the effects of environmental xenobiotics. This group of substances includes micro- and nanoplastics (MNPs) as well as trace elements. This literature review summarises the current knowledge on the individual and combined effects of MNPs and trace elements—including essential bioelements (zinc (Zn), selenium (Se), copper (Cu), chromium (Cr), manganese (Mn)) and toxic elements (cadmium (Cd), Lead (Pb), arsenic (As), mercury (Hg))—on ovarian physiology and clinical conditions such as polycystic ovary syndrome (PCOS), gonadal dysfunction and infertility. Essential trace elements play irreplaceable roles as enzyme cofactors (e.g., superoxide dismutase (SOD), glutathione peroxidase (GPX)) and transcriptional regulators; however, their biological action is confined to a narrow homeostatic window, within which both deficiency and excess disrupt cellular redox status and the hypothalamic–pituitary –gonadal axis. The effect of toxic heavy metals is different; these exhibit threshold-independent cytotoxic, genotoxic and endocrine-disrupting effects, inducing apoptosis of granulosa cells, endoplasmic reticulum stress and the silencing of steroidogenic genes (e.g., Steroidogenic acute regulatory protein (StAR), CYP11A1, CYP19A1) via epigenetic modifications, which accelerates the depletion of the ovarian reserve (measured by a decline in anti-Müllerian hormone (AMH)). Concurrently, MNPs overcome biological barriers and accumulate within the ovarian microenvironment, thereby inducing reactive oxygen species (ROS)-dependent apoptosis, NLR family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis, cytoskeletal disruption, and tissue fibrosis. A key element of this review is the identification of mechanistic convergence and potential toxic synergism between MNPs and heavy metals. Co-exposure enhances toxin retention within cells by inhibiting ATP-binding cassette (ABC) transporters, potentiates mitochondrial depolarisation, and activates protein kinase RNA-like endoplasmic reticulum kinase–eukaryotic translation initiation factor 2 alpha (PERK/eIF2α) stress signalling. Understanding these shared molecular pathways forms the basis for assessing multi-component risk in female reproductive toxicology and for developing targeted protective strategies.

The pancreas is an organ with two functions: endocrine and exocrine. The proper functioning of the pancreas depends on many factors. One of these is trace elements—precise control of trace element homeostasis is important for both the endocrine and exocrine parts. This review provides a comprehensive summary of current knowledge regarding the role of trace elements: iron (Fe), copper (Cu), cobalt (Co), iodine (I), manganese (Mn), zinc (Zn), silver (Ag), cadmium (Cd), mercury (Hg), lead (Pb), and selenium (Se) in pancreatic physiology and their influence on the pathogenesis of key diseases of this organ, such as diabetes (DM), acute (AP) and chronic pancreatitis (CP), autoimmune pancreatitis (AIP), and pancreatic cancer (PC). Trace elements, including Fe, Cu, Zn, Se, and Mn, play a fundamental role in maintaining endocrine and exocrine homeostasis, participating in insulin synthesis, stabilizing digestive enzymes, and the functioning of antioxidant systems. It has been demonstrated that disturbances in their concentrations lead to the activation of pathological molecular pathways, including oxidative stress, chronic inflammation, and beta-cell apoptosis. In the context of diabetes, excess Fe promotes ferroptosis, whilst exposure to heavy metals such as Cd, Pb, and Hg induces insulin resistance and pancreatic islet dysfunction. In the course of pancreatitis, elements such as Zn and Se exhibit protective potential by stabilizing tissue barriers, whereas toxic metals impair ion transport, exacerbating fibrotic processes. Furthermore, analysis of available data indicates a significant association between heavy metal accumulation and pancreatic carcinogenesis, driven by DNA damage and oncogene modulation. Understanding pancreatic metallomics opens new prospects for early diagnosis, environmental prevention, and the development of targeted therapeutic strategies that restore the body’s micronutrient balance.