Toxicity effects of disinfection byproduct chloroacetic acid to Microcystis aeruginosa: Cytotoxicity and mechanisms.

Chlorine-based disinfectants are widely used for disinfection in wastewater treatment. The mechanism of the effects of chlorinated disinfection by-products on cyanobacteria was unclear. Herein, the physiological effects of chloroacetic acid (CAA) on Microcystis aeruginosa (M. aeruginosa), including acute toxicity, oxidative stress, apoptosis, production of microcystin-LR (MC-LR), and the microcystin transportation-related gene mcyH transcript abundance have been investigated. CAA exposure resulted in a significant change in the cell ultrastructure, including thylakoid damage, disappearance of nucleoid, production of gas vacuoles, increase in starch granule, accumulation of lipid droplets, and disruption of cytoplasm membranes. Meanwhile, the apoptosis rate of M. aeruginosa increased with CAA concentration. The production of MC-LR was affected by CAA, and the transcript abundance of mcyH decreased. Our results suggested that CAA poses acute toxicity to M. aeruginosa, and it could cause oxidative damage, stimulate MC-LR production, and damage cell ultrastructure. This study may provide information about the minimum concentration of CAA in the water environment, which is safe for aquatic organisms, especially during the global coronavirus disease 2019 pandemic period.

Barrier function and ultrastructure characteristics of epidermis in patients with primary cutaneous amyloidosis.

Previous studies on primary cutaneous amyloidosis (PCA) have mainly focused on exploring genetic mutation and components of amyloid in patients with PCA. However, studies on skin barrier function in PCA patients are scarce. Here, we detected the skin barrier function in PCA patients and healthy people by using noninvasive techniques and characterized ultrastructural features of PCA lesions compared with healthy people using transmission electron microscopy (TEM). The expression of proteins related to skin barrier function was examined by immunohistochemistry staining. A total of 191 patients with clinically diagnosed PCA and 168 healthy individuals were enrolled in the study. Our analysis revealed that all investigated lesion areas displayed higher transepidermal water loss and pH values, and lower Sebum levels and stratum corneum hydration levels in PCA patients compared with the same site area in healthy individuals. The TEM results showed that the intercellular spaces between the basal cells were enlarged and the number of hemidesmosomes decreased in PCA lesions. Immunohistochemical staining showed that the expression of integrin α6 and E-cadherin in PCA patients was less than that in healthy controls, while no differences in the expression of loricrin and filaggrin were observed. Our study revealed that individuals with PCA displayed skin barrier dysfunction, which may be related to alterations in epidermal ultrastructure and a decrease in the skin barrier-related protein E-cadherin. However, the molecular mechanisms underlying skin barrier dysfunction in PCA remain to be elucidated.