Copyright@ Silvia Santillo | Biomed J Sci & Tech Res| BJSTR. MS.ID.003252. 14094 Research Article ISSN: 2574 -1241 Membrane Currents in Madin-Darby Bovine Kidney Cells are Enhanced by Exposure to Dioxin Silvia Santillo* 1 , Filomena Fiorito 2 and Luisa De Martino 3 1 Istituto di Scienze Applicate e Sistemi Intelligenti del CNR (ISASI-CNR), Naples, Italy 2 Istituto Zooprofilattico Sperimentale del Mezzogiorno, Portici, Naples, Italy 3 Dipartimento di Medicina Veterinaria e Produzioni Animali, Università degli Studi di Napoli Federico II, Naples, Italy *Corresponding author: Silvia Santillo, Istituto di Scienze Applicate e Sistemi Intelligenti del CNR (ISASI-CNR), Naples, Italy DOI: 10.26717/BJSTR.2019.19.003252 Introduction The name ”dioxins” is used to indicate a great family of struc- turally and chemically related Polychlorinated-Dibenzo-P-Dioxins (PCDDs) and Polychlorinated-Dibenzofurans (PCDFs). They are environmental toxins of current interest [1] as they can bio-accu- mulate in food chain, due to their lipophilic nature. The most tox- ic 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 chlorac- ne, liver damage, disruption of hormone signaling pathways, repro- ductive 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 Interna- tional Agency for Research on Cancer [9]. In vitro studies have shown TCDD neurotoxicity in mouse cer- ebellar 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 mecha- nism of action responsible of TCDD biochemical effects is the AhR stimulation. Through Aryl Hydrocarbon Receptor Nuclear Trans- locator (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, Mo- rales-Hernandez et al. [15] have related TCDD toxicity to a disrup- tion 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 re- sponses 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 auto- phagy [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 ex- ample, 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 elec- Received: June 18, 2019 Published: June 24, 2019 Citation: Silvia Santillo, Filomena Fior- ito, Luisa De Martino. Membrane Cur- rents in Madin-Darby Bovine Kidney Cells are Enhanced by Exposure to Diox- in. Biomed J Sci & Tech Res 19(1)-2019. BJSTR. MS.ID.003252. ARTICLE INFO 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- tetrachlorodiben- zo-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. Keywords: MDBK; Voltage-gated ion channels; TCDD; Whole cell patch-clamp