Analysis of Cadmium, Epigallocatechin Gallate, and Vitamin C Co-exposure on PC12 Cellular Mechanisms

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 -asco...

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Bibliographic Details
Published in:Biological trace element research 2020-12, Vol.198 (2), p.627-635
Main Authors: Bondad, Serene Ezra C., Kurasaki, Masaaki
Format: Article
Language:English
Subjects:
Acids
Antagonism
Antioxidants
Apoptosis
Ascorbic acid
Autophagy
Biochemistry
Biological stress
Biomedical and Life Sciences
Biotechnology
Cadmium
Caspase-9
Cell death
Cell membranes
Cell survival
Cytotoxicity
Damage
Diet
Epigallocatechin gallate
Health risks
Life Sciences
Nutrition
Oncology
Oxidants
Oxidative stress
Oxidizing agents
p53 Protein
Pheochromocytoma cells
Proteins
Risk analysis
Risk factors
Survival
Toxicity
Vitamin C
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Summary: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 l -ascorbic 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.
ISSN:0163-4984
1559-0720
DOI:10.1007/s12011-020-02097-9