Analysis of Cadmium, Epigallocatechin Gallate, and Vitamin C Co-exposure on PC12 Cellular Mechanisms
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Analysis of Cadmium, Epigallocatechin Gallate, and Vitamin C Co-exposure on PC12 Cellular Mechanisms Serene Ezra C. Bondad 1 & Masaaki Kurasaki 1,2 Received: 19 November 2019 / Accepted: 25 February 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Exposure to cadmium (Cd) is a risk factor to health impairments, wherein its cytotoxicity is attributed to induction of oxidative stress. Usage of anti-oxidants, however, can help lessen the damaging effects of Cd. The effect of Cd interaction with low concentration of dietary anti-oxidants, L-ascorbic acid and (−)-epigallocatechin gallate (EGCG), to PC12 cellular mechanisms was examined. The expected toxicity of Cd was observed on PC12 cells but addition of L-ascorbic acid ameliorated this effect. On the other hand, addition of EGCG was able to increase the cytotoxicity of Cd and to decrease the protective effect of Lascorbic acid against Cd. Increase in LDH activity and decrease in free sulfhydryl levels indicated cell membrane damage and oxidative stress, respectively, in Cd- and EGCG-Cd-treated cells. Downregulation of pro-apoptotic proteins (pro-caspase-9, p53, and ERK1) was observed in cells treated with Cd alone and EGCG-Cd, while upregulation of autophagy-linked proteins (p62 and pBeclin1) was found on L-ascorbic acid–Cd combination treatments. These findings indicate that Cd causes cells to undergo an autophagy-enhanced cell death; low-concentration EGCG and L-ascorbic acid promotes cell survival individually; however, interaction of EGCG with Cd showed enhancement of Cd toxicity and antagonism of L-ascorbic acid efficiency. Keywords Apoptosis . Autophagy . Cadmium . Epigallocatechin gallate . Oxidative stress . Vitamin C
Abbreviations Akt Protein kinase B Bax BCl2-associated X apoptosis regulator EGCG (−)-Epigallocatechin-3-gallate ERK1 Extracellular signal–regulated kinase-1 GSH Glutathione LDH Lactate dehydrogenase mTOR Mammalian target of rapamycin PBS Phosphate buffer saline ROS Reactive oxygen species SEM Standard error of mean SH Thiol group
* Masaaki Kurasaki [email protected] Serene Ezra C. Bondad [email protected] 1
Graduate School of Environmental Science, Hokkaido University, Sapporo 060-0810, Japan
2
Faculty of Environmental Earth Science, Hokkaido University, Sapporo 060-0810, Japan
Introduction Exposure to low-concentration cadmium (Cd) has been linked to disorders in the renal, nervous, reproductive, skeletal, and hepatic systems, in both humans and animals [1]. Dietary sources and cigarette smoking are the most common means for humans to be chronically exposed to low-concentration Cd [2]. With a biological half-life of 10–30 years, Cd is not easily excreted from the human body and accumulates mainly in the liver and kidney [3]. The cytotoxicity of Cd has been mainly attributed to its production of reactive oxygen species (ROS) which results to an imbalance of the cell’s homeostasis, eventually leading to oxidative stress [4, 5]. When it comes to ameliorating toxicities, chemicals from food are of pa
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