Silicon dioxide-induced endoplasmic reticulum stress of alveolar macrophages and its role on the formation of silicosis fibrosis: a review article.

Silicosis is a chronic lung inflammatory disease induced by long-term inhalation of high concentrations of silicon dioxide (SiO), characterized by pulmonary fibrosis. Inhalation of silica invades alveolar macrophages (AMs) and changes the micro-environment of the cell, resulting in abnormal morphology and dysfunction of the endoplasmic reticulum (ER). Once beyond the range of cell regulation, the endoplasmic reticulum stress (ERS) will occur, which will lead to cell damage, necrosis, and apoptosis, eventually causing silicosis fibrosis through various mechanisms.

Altered M1/M2 polarization of alveolar macrophages is involved in the pathological responses of acute silicosis in rats in vivo.

Alveolar macrophages play a vital role in the development of acute silicosis, but the dynamic changes of M1 and/or M2 phenotypes have not been elucidated. In this study, acute silicosis models of rat were established by a one-time dusting method, and the rats were sacrificed after 1, 3, 7, 14, and 28 days. The polarity states of macrophages were assessed by measuring the M1/M2 marker genes of alveolar macrophages and the M1/M2 marker proteins in bronchoalveolar lavage fluid.

Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO-induced pulmonary fibrosis in rats .

Silicosis is a serious occupational disease characterized by pulmonary fibrosis, and its mechanism and progression have not been fully elucidated yet. In this study, silicosis models of rat were established by a one-time dusting method, and the rats were sacrificed after 30, 60, and 120 days (herein referred to as the 30, 60, and 120 days groups, respectively). The rats without dust exposure were used as the control.

Effects of abnormal expression of fusion and fission genes on the morphology and function of lung macrophage mitochondria in SiO-induced silicosis fibrosis in rats in vivo.

Silicosis is a serious occupational disease affecting millions of related workers. Many studies showed lung macrophages play an important role in the disease. However, the changes of macrophages are not fully characterized and the mechanisms need further investigations.

[Effects of malathion on testicular spermatogenic function in rats].

Objective: To investigate the effects of malathion on the testicular spermatogenic function of male rats and its working mechanism.

Methods: Forty specific pathogen-free male Wistar rats were randomly and equally divided into four groups: three exposure groups and a control group. Malathion was administered orally to male rats in the exposure groups at 33.

[Association between GSTP1, GSTM1, GSTT1 genetic polymorphisms and urinary styrene phenyl hydroxyethyl mercapturic acids level].

Objective: To investigate the relationship between genetic polymorphisms of glutathione S-transferase P1 (GSTP1), glutathione S-transferase M1 (GSTM1), and glutathione S-transferase T1 (GSTT1) and urinary level of mercapturic acids of styrene (PHEMAs) in workers exposed to styrene.

Methods: One hundred and twenty-six workers exposed to styrene were selected as exposure group, and 150 workers without styrene exposure as the control group; all the workers came from a locomotive shell production factory in Shandong Province, China. The PCR-RFLP technique was applied to analyze the individual genetic polymorphisms of GSTP1; the multiplex PCR technique was used to investigate the genetic polymorphisms of GSTM1 and GSTT1; the relationship between genetic polymorphisms of GSTP1, GSTM1, and GSTT1 and urinary level of PHEMAs in workers exposed to styrene was statistically analyzed.