Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes

Abstract

Samples of environmental particulate matter (PM) contain environmentally persistent free radicals (EPFRs) capable of sustained generation of oxygen radicals. While exposure to EPFRs produces cardiac toxicity and oxidative stress in experimental animals, the underlying mechanisms are largely unknown. To determine whether EPFRs could directly damage cardiomyocytes, cultured mouse cardiomyocytes (HL-1) and primary rat adult left ventricular myocytes (ALVM) were incubated with an EPFR consisting of 1, 2-dichlorobenzene chemisorbed to CuO-coated silica beads (DCB230). Treatment with DCB230 killed both HL-1 and ALVM in a dose- and time-dependent manner. The cytotoxic effects of DCB230 were significantly attenuated by treatment with α-tocopherol. One to 2 hours after exposure to DCB230, there were significant reductions in mitochondrial membrane potential and significant increases in cleaved caspase-9, but no significant increases in DNA damage or cell death. After 8 hours of treatment, there were significant increases in caspase-3, caspase-9, DNA damage and PARP cleavage associated with significant cell death. Together, these data indicate that DCB230 kills HL-1 myocytes by inducing oxidative stress that initiates apoptosis, with the intrinsic or mitochondrial pathway acting early in the apoptotic signaling process.

Correlation between persistent free radicals of biochar and bio-oil yield at different pyrolysis temperatures

“…Studies have shown that thermal processes, such as biomass burning, coal combustion, and metallurgical industries, can produce EPFRs. These EPFRs can induce the production of free radicals, such as HO•, in the body, causing the biomolecules in the body to be oxidized and then causing DNA damage in the body (Chuang et al 2017).…”

Transformation of Polycyclic Aromatic Hydrocarbons and Formation of Environmentally Persistent Free Radicals on Modified Montmorillonite: The Role of Surface Metal Ions and Polycyclic Aromatic Hydrocarbon Molecular Properties

“…Atmospheric particles, soil, and sediments that are co-contaminated with toxic metals and polycyclic aromatic hydrocarbons (PAHs) have raised concerns due to their potential to cause combined adverse effects on human and ecological health. − The co-presence of toxic metals, especially some transition metals, may also change the particle properties, which, in turn, affects the transport, fate, and toxicity of PAHs and other organic pollutants. , For example, particulate matter containing chlorophenol and transition metal ions emitted from combustion sources in the atmosphere produces environmentally persistent free radicals (EPFRs) that may increase the human health risk of developing respiratory and cardiopulmonary diseases. − These types of EPFRs could also be observed during the oxidative decomposition of aromatic compounds (e.g., catechol and dibenzofuran). , The formation of EPFRs and their ecotoxicological effects in the natural environment have attracted increasing attention from scientists and public-health decision makers. , Fly ash and particulate matter contain organic contaminants and transition metals. As such, several studies have been conducted to understand combustion-related EPFRs on metal and mineral surfaces. − The role of transition-metal oxides on organic-contaminated surfaces in the formation and stabilization of combustion-generated EPFRs has been explored. − Progress has been made in these systems to characterize the electron transfer from organic molecules, especially chloro- and hydroxyl-substituted benzenes, to the metal and silica surfaces, resulting in the formation of EPFRs. − Comparatively, only limited studies have been performed examining the formation of EPFRs and their stabilization on contaminated soils at room temperature and also under environmental conditions. − …”

CBL knockdown protects cardiomyocytes against hypoxia‑reoxygenation injury by downregulating GRB2 expression

“…Mitochondria are vital for the production of ATP and the induction of cell apoptosis ( 44 ). Cytochrome c , a marker of activation of the mitochondrial apoptosis pathway, can activate pro-caspase 9, thereby promoting the activation of caspase-3( 45 ). In addition, Bax is a pro-apoptotic protein ( 46 ).…”