Drug-induced osteoporosis and mechanisms of bone tissue regeneration through trace elements.

Osteoporosis is associated with an imbalance in bone formation, with certain drugs used in disease treatment being implicated in its development. Supplementation with trace elements may contribute to bone regeneration, offering an alternative approach by enhancing bone mineral density (BMD) and thereby thwarting the onset of osteoporosis. This review aims to assess the mechanisms through which trace elements such as copper (Cu), iron (Fe), selenium (Se), manganese (Mn), and zinc (Zn) are linked to increased bone mass, thus mitigating the effects of pharmaceuticals. Our findings underscore that the use of drugs such as aromatase inhibitors (AIs), proton pump inhibitors (PPIs), antiretrovirals, glucocorticoids, opioids, or anticonvulsants can result in decreased BMD, a primary contributor to osteoporosis. Research indicates that essential elements like Cu, Fe, Se, Mn, and Zn, through various mechanisms, can bolster BMD and forestall the onset of the disease, owing to their protective effects. Consequently, our study recommends a minimum daily intake of these essential minerals for patients undergoing treatment with the aforementioned drugs, as the diverse mechanisms governing the effects of trace elements Cu, Fe, Mn, Se, and Zn facilitate bone remodeling.

Teratogenic effects of the dicamba herbicide in Zebrafish (Danio rerio) embryos.

Dicamba has been used worldwide for 60 years, but few studies have been conducted on its environmental safety and health effects. Therefore, this study aims to evaluate the acute toxicity, teratogenic effects, oxidative stress, and neurotoxicity of Dicamba in zebrafish embryos. Embryos were exposed to concentrations of 4.5, 18, 72, and 288 mg/L of Dicamba for 96 h. Among the teratogenic effects, yolk sac edema predominated, besides malabsorption of nutrients (grayish yolk sac). The presence of edema may indicate problems with circulation and water efflux from the embryos, which may be related to kidney and cardiovascular problems. Other effects such as hemorrhage, spinal and eye malformations, and dwarfism were also observed. The hatching rate was reduced in the highest concentration, and in the other concentrations, a decrease was noticeable indicating a delay in development. Neurotoxic effects were also observed. Oxidative stress analysis showed a significant decrease in SOD at all concentrations and an increase in GPx, GSH, and LPO at 288 mg/L of Dicamba. It was observed that the herbicide is capable of causing teratogenic effects, developmental delay, and oxidative stress. These results show that exposure to Dicamba, in a commercial formulation, can bring risks during embryonic development. In addition, it highlights the need for further studies on the effects of the herbicide and a reassessment of toxicity categorization.