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Protective effect of selenomethionine on aflatoxin B1-induced oxidative stress in MDCK cells
Fahmida Parveen1, Zaheer Ahmed Nizamani, Fang Gan
1Institute of Nutritional and Metabolic Disorders in Domestic Animals and Fowls, Nanjing Agricultural University, Nanjing, 210095, China.
Abstract:
AFB1 is a mycotoxin which exerts their cytotoxicity through increasing oxidative damage in target organ. Kidney is one of target organs vulnerable to damage caused by AFB1. In this study, Madin-Darby canine kidney (MDCK) cells were used to evaluate the AFB1-induced cell damage by the MTT assay. The results revealed that the toxic effect of AFB1 on MDCK cells is both dose and time dependent. Half maximal toxic concentration (IC50) was noted at 0.25 μg/ml of AFB1. Further, protective effect of six different concentrations (0.2, 0.8, 1, 2, 4, and 8 μM) of selenomethionine (SeMet) was observed against 0.25 μg/ml of AFB1-induced damage. The results showed that 0.25 μg/ml of AFB1 caused significant increase in oxidative stress, which was demonstrated by significant increase of malondialdehyde (MDA) level, reduction of intracellular GSH level, as well as GPX1 activity and mRNA level in MDCK cells when compared with control. SeMet protected the cells from AFB1-induced oxidative damage in a dose-dependant manner. Good protection could be achieved between 1 and 4 μM of concentration. Amid this range, MDA level significantly decreased while intracellular GSH level and GPX1 activity in addition to mRNA level significantly increased. Moreover, cell viability was significantly improved. It could be concluded that SeMet is a potential antioxidative agent to alleviate AFB1-induced oxidative stress.
Insights
Selenomethionine (SeMet) protects kidney cells from aflatoxin B1 (AFB1)-induced oxidative damage. SeMet effectively reduced oxidative stress markers and improved cell viability, showing its potential as an antioxidant against AFB1 toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Nutritional Science
Background:
- Aflatoxin B1 (AFB1) is a mycotoxin that causes cytotoxicity by increasing oxidative damage in target organs, including the kidney.
- Madin-Darby canine kidney (MDCK) cells are susceptible to AFB1-induced damage.
Purpose of the Study:
- To evaluate the protective effect of selenomethionine (SeMet) against AFB1-induced oxidative stress and cell damage in MDCK cells.
- To determine the dose-dependent efficacy of SeMet in mitigating AFB1 toxicity.
Main Methods:
- MTT assay was used to assess cell viability and toxicity.
- Measurement of malondialdehyde (MDA) levels, intracellular glutathione (GSH) levels, and glutathione peroxidase 1 (GPX1) activity and mRNA levels to evaluate oxidative stress.
- Exposure of MDCK cells to AFB1 and varying concentrations of SeMet.
Main Results:
- AFB1 exposure significantly increased oxidative stress markers (MDA, decreased GSH, reduced GPX1 activity/mRNA) and decreased cell viability in MDCK cells.
- SeMet demonstrated a dose-dependent protective effect against AFB1-induced damage, with optimal protection observed between 1 and 4 μM.
- SeMet treatment significantly reversed the effects of AFB1, decreasing MDA and increasing GSH levels, GPX1 activity, mRNA levels, and overall cell viability.
Conclusions:
- Selenomethionine is a potent antioxidant capable of alleviating AFB1-induced oxidative stress and cellular damage in kidney cells.
- SeMet shows promise as a therapeutic or preventative agent against mycotoxin-induced kidney injury.
