Despite the effectiveness of doxorubicin as a chemotherapeutic agent, it exerts toxicity on non-target organs, including the male reproductive organs. This review synthesizes current evidence on both ferroptotic and non-ferroptotic mechanisms underlying doxorubicin (DOX)-induced male reproductive dysfunction. DOX disrupts testicular function by inducing oxidative stress, lipid peroxidation, mitochondrial dysfunction, and apoptosis, particularly in Leydig, Sertoli, and spermatogenic cells.
View Article and Find Full Text PDF: The presence of antibiotic residues in the aquatic environment is a likely contributor to the current increase in antibiotic resistance, posing a significant threat to global health. This study investigated the use of a low-cost and sustainable material based on sawdust with the purpose of removing rifampicin residues from water. : The sawdust was pretreated with 2M sulfuric acid and was characterized using Fourier Transform Infrared spectroscopy (FT-IR), a Mastersizer, scanning electron microscopy (SEM), an elemental analyser, and the pH point of zero charge (pH).
View Article and Find Full Text PDFGlobally, among ready-to-eat (RTE) vegetables, lettuce is well-known as a potential host for Enterobacteriaceae, which theatens public health. However, in addition to E. coli, pathogenic Enterobacter species associated with RTE lettuce is poorly investigated, as well as their genetic relationship with sources of contamination has not been determined.
View Article and Find Full Text PDFErectile dysfunction (ED), which is defined as the inability to attain and maintain a satisfactory penile erection to sufficiently permit sexual intercourse, is a consequence and also a cause of cardiometabolic disorders like diabetes mellitus, systemic hypertension, central obesity, and dyslipidemia. Although there are mounting and convincing pieces of evidence in the literature linking ED and cardiometabolic disorders, impairment of nitric oxide-dependent vasodilatation seems to be the primary signaling pathway. Studies have also implicated the suppression of circulating testosterone, increased endothelin-1, and hyperactivation of Ang II/ATIr in the pathogenesis of ED and cardiometabolic disorders.
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