Membrane Currents in Madin-Darby Bovine Kidney Cells are Enhanced by Exposure to Dioxin
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2019, Vol 19, Issue 1
Abstract
Madin-Darby bovine kidney cells, which are known to be responsive to the effect of dioxin, have to been used to investigate if exposure to the 2,3,7,8- tetrachlorodibenzo- p-dioxin could alter their membrane currents. Herein, we present preliminary results showing that this chemical modifies ionic membrane currents and that the modification mainly involves the chloride current component.The name ”dioxins” is used to indicate a great family of structurally and chemically related Polychlorinated-Dibenzo-P-Dioxins (PCDDs) and Polychlorinated-Dibenzofurans (PCDFs). They are environmental toxins of current interest [1] as they can bio-accumulate in food chain, due to their lipophilic nature. The most toxic of these compounds is the 2,3,7,8-Tetrachlorodibenzo-P-Dioxin (TCDD). This chemical, commonly known as dioxin, can cause a wide range of tissue- and species-specific toxic effects, as chloracne, liver damage, disruption of hormone signaling pathways, reproductive and developmental defects [2-4]. Indeed, dioxin can alter brain development, produce cognitive disability, motor dysfunction [5,6], and also induce important alterations in neurodevelopment of human newborns following gestational exposure [7]. Moreover, TCDD may provoke immunosuppression and leads to an increased susceptibility to infectious agents [4,8]. Although the molecular mechanisms for carcinogenicity by dioxin have not been clarified, in 1997 TCDD was classified as a cancer promoter by the International Agency for Research on Cancer [9]. In vitro studies have shown TCDD neurotoxicity in mouse cerebellar granule cells, cortical neurons [10,11] and in NGF- differen tiated PC12 cells [12]. The toxicity of TCDD has been attributed to different mechanisms. In vertebrates, the main molecular mechanism of action responsible of TCDD biochemical effects is the AhR stimulation. Through Aryl Hydrocarbon Receptor Nuclear Translocator (ARNT), the AhR/ARNT complex translocates into nucleus where it promotes various AhR-responsive genes activating their transcription [13,14]. In human SH-SY5Y neuronal cell line, Morales- Hernandez et al. [15] have related TCDD toxicity to a disruption of calcium homeostasis while others [16-18] have established that the Aryl Hydrocarbon Receptor (AhR), to which TCDD binds with a high affinity, is involved in mediating the diverse toxic responses of this dioxin. In Madin-Darby Bovine Kidney (MDBK), an epithelial cell line, through AhR [19,20], TCDD induced a significant cell proliferation [21], increased the incidence cell death with autophagy [19,20,22] and promoted the Bovine Herpesvirus-1 (BoHV- 1) infection as well as BoHV-1-induced apoptosis [4,19-21,23-25]. However, data from literature are sometimes contrasting. For example, the effect on apoptosis signaling can result, dependent on the cell contest, either inducing [19,20] and repressing [17]. Very few are the studies that report effects on the membrane electrical activity after TCDD exposure [26]. The membrane electrical activity is due to the influx/efflux of ions across ion channels and pumps. It regulates the homeosta- sis of the cell [27] and many fundamental processes like as autophagy [28] and apoptosis [29] that also result to be very sensitive to TCDD [4,19-25].
Authors and Affiliations
Silvia Santillo, Filomena Fiorito, Luisa De Martino
Keywords
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- EP ID EP622406
- DOI 10.26717/BJSTR.2019.19.003252
- Views 191
- Downloads 0
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