Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death

Abstract

Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.

Antiapototic Effect of Captopril in Cisplatin - Induced Kidney Injury in Rats

“…The co-existence of both radicals forms peroxynitrite, a potent RNS [39] . Both ROS and RNS are capable to activate the intrinsic apoptotic pathway to ultimately cleave Casp-3 [40] . In the present work, captopril antiapoptotic capacity might be a function of its antioxidtive and antinitroactive stress activities evident by the reduction in lipid peroxidation and NO that was associated by the elevation of the antioxidants GSH, GPx, SOD, and CAT, effects that support previous studies in the different models [13,41,42] .…”

Health effects of desalinated water: Role of electrolyte disturbance in cancer development

“…The cellular effects of electrolyte dysfunction are, in a sense, similar to those of exposure to many low-dose environmental carcinogens which can elicit both pro-and anti-apoptotic effects on cells depending on the cell type (Langie et al, 2015;Narayanan et al, 2015). As with exposure to low-dose carcinogens, damage of the DNA by osmotic stress or electrolyte dysregulation can lead to two outcomes.…”

“…diesel exhaust) that could be shown to be 'complete' carcinogens (i.e., substances that could cause cancer on their own). Advances in cancer biology subsequently revealed the limitations of this approach and have let to the multistage and "hallmarks of cancer" framework which recognizes that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce tumors and ultimately malignancies (Casey et al, 2015;Hu et al, 2015;Narayanan et al, 2015). We hypothesize that electrolyte disturbance from exposure to demineralized water can mediate the cancer microenvironment in ways that lead to procarcinogenic outcomes.…”

Perspectives on the specific targeting of Fusarium graminearum for the development of alternative head blight treatment approaches

“…As an example, chlorothalonil was shown to influence bacterial growth in soil and this may influence nitrogen cycling in the ecosystem (Černohlávková et al ., ). In addition, chlorothalonil is a possible inducer of cytochrome P450, ErbB‐2 tyrosine kinase and MAP kinase, leading to increased cell proliferation in tumour cells, as well as increasing the risk of resistance of tumours to treatment and survival of tumour cells (Narayanan et al ., ).…”

“…; Edwards, ; Fisher et al ., ; Kane et al ., ). Finally, growing understanding of the interactions between increased usage of existing fungicides and the environment highlights the possibility of significant environmental damage (Yang et al ., ; Narayanan et al ., ; David et al ., ).…”