Main Group and Transition Metal-Mediated Phosphaalkene Insertion Reactions Initiated by Phosphines Containing Si–P Bond

Bani‐Fwaz, Mutasem Z.

doi:10.1080/02603594.2020.1837783

Cited by 1 publication

(1 citation statement)

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“…Over 200 million people are exposed to arsenic and its toxicity, and its concentration in groundwater exceeds the limit level for drinking water (10 μg/L) set by the WHO as well as the Environmental Protection Agency of the United States in more than 35 countries across the globe. 1 Though recently more and more arsenic derivatives and its compounds are being synthesized and discovered, and some of them are used in the treatment of cancer (especially leukemia), 2,3 as a result of long-term exposure, arsenic can enter and accumulate in the body via the respiratory tract, digestive tract, and skin contact, causing arsenic poisoning. Moreover, prolonged exposure to arsenic can cause severe medical conditions, including diabetes, high blood pressure, cardiovascular disease, neurological disease, and cancer.…”

Section: Introductionmentioning

confidence: 99%

Cathepsin B mediates the lysosomal-mitochondrial apoptosis pathway in arsenic-induced microglial cell injury

Zhang

Jiang

et al. 2023

Hum Exp Toxicol

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Arsenic is a prevalent environmental pollutant that targets the nervous system of living beings. Recent studies indicated that microglial injury could contribute to neuroinflammation and is associated with neuronal damage. Nevertheless, the neurotoxic mechanism underlying the arsenic-induced microglial injury requires additional research. This study explores whether cathepsin B promotes microglia cell damage caused by NaAsO2. Through CCK-8 assay and Annexin V-FITC and PI staining, we discovered that NaAsO2 induced apoptosis in BV2 cells (a microglia cell line). NaAsO2 was verified to increase mitochondrial membrane permeabilization (MMP) and promote the generation of reactive oxygen species (ROS) through JC-1 staining and DCFDA assay, respectively. Mechanically, NaAsO2 was indicated to increase the expression of cathepsin B, which could stimulate pro-apoptotic molecule Bid into the activated form, tBid, and increase lysosomal membrane permeabilization by Immunofluorescence and Western blot assessment. Subsequently, apoptotic signaling downstream of increased mitochondrial membrane permeabilization was activated, promoting caspase activation and microglial apoptosis. Cathepsin B inhibitor CA074-Me could mitigate the damage of microglial. In general, we found that NaAsO2 induced microglia apoptosis and depended on the role of the cathepsin B-mediated lysosomal-mitochondrial apoptosis pathway. Our findings provided new insight into NaAsO2-induced neurological damage.

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Section: Introductionmentioning

confidence: 99%