Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease.

Copper is a toxic heavy metal that causes various damage when it accumulates in the body beyond the physiological threshold. Wilson disease (WD) is an inherited disorder characterized by impaired copper metabolism. Reproductive damage in male patients with WD is gradually attracting attention.

A retrospective cohort study: vaccination status and safety analysis of SARS-CoV-2 vaccine in patients with Wilson's disease.

Background: Wilson's disease (WD) is a rare hepatic and neurological disorder, which can dramatically worsen by traumatic injuries, surgeries, and infections. No studies have reported safety data of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination in WD patients. We aimed to investigate the SARS-CoV-2 vaccination status and post-vaccination adverse events in WD patients.

Glutathione improves testicular spermatogenesis through inhibiting oxidative stress, mitochondrial damage, and apoptosis induced by copper deposition in mice with Wilson disease.

Background And Objective: There are considerable evidence of reproductive impairment in male organisms with Wilson disease (WD). The purpose of this study was to observe spermatogenesis, mitochondrial damage, apoptosis, and the level of oxidative stress in the testes of Wilson disease model TX mice, and to observe the effect and mechanism of glutathione on testicular spermatogenesis.

Methods: Mice were divided into a normal control group (control group), Wilson disease model TX mice group (WD group), penicillamine-treated TX mice group (penicillamine group) and glutathione-treated TX mice group (glutathione group).