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Protective effects of selenium on aflatoxin B1-induced mitochondrial permeability transition, DNA damage, and
Dayou Shi1, Shenquan Liao, Shining Guo
1College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Abstract:
Aflatoxin B1 (AFB1) is a mycotoxin that causes cytotoxicity through oxidative damage to its target organs. The liver is the first target of AFB1 damage. The aim of this study was to evaluate the protective effect of selenium on AFB1-induced hepatic mitochondrial damage in ducklings using molecular biological and histopathological techniques. Aflatoxin was administered via intragastric intubation (0.1 mg/kg body weight), daily for 21 days. The experimental group also received intragastric sodium selenite (1 mg/kg body weight), while the control group was given the same volume of dimethyl sulfoxide (DMSO). Sequence analysis of the mitochondrial DNA D-loop region showed that AFB1 induced damage. All AFB1-administrated ducklings were identified as having D-loop mitochondrial DNA mutations. Mutations were detected in two ducklings that had received both AFB1 and selenium. Mitochondrial swelling assays showed that opening of the mitochondrial permeability transition pores was increased in ducklings that had received AFB1 for 14 and 21 days (P < 0.05). Selenium significantly attenuated these adverse effects of AFB1. After AFB1 exposure, histological alterations were observed, including fat necrosis, steatosis, and formation of lymphoid nodules with infiltrated lymphocytes. These histological abnormalities were also attenuated by treatment with selenium. The overall data indicated that selenium exerts a potent protective effect against AFB1-induced hepatic mitochondrial damage, possibly through its antioxidant activity.
Insights
Selenium protects ducklings from liver damage caused by Aflatoxin B1 (AFB1). This study shows selenium can prevent AFB1-induced mitochondrial DNA mutations and liver abnormalities, highlighting its antioxidant role.
Area of Science:
- Toxicology
- Mitochondrial Biology
- Nutritional Biochemistry
Background:
- Aflatoxin B1 (AFB1) is a potent mycotoxin causing liver damage via oxidative stress.
- Hepatic mitochondria are primary targets for AFB1-induced cytotoxicity.
- Understanding protective mechanisms against AFB1 toxicity is crucial for animal health.
Purpose of the Study:
- To investigate the protective effects of selenium against AFB1-induced hepatic mitochondrial damage in ducklings.
- To elucidate the molecular and histopathological changes associated with AFB1 exposure and selenium intervention.
Main Methods:
- Ducklings were administered AFB1 (0.1 mg/kg) daily for 21 days.
- Experimental groups received sodium selenite (1 mg/kg) concurrently with AFB1.
- Molecular analysis (mtDNA D-loop sequencing) and histopathological examination were performed.
Main Results:
- AFB1 exposure induced significant mutations in the mitochondrial DNA D-loop region.
- Increased mitochondrial permeability transition pore opening was observed in AFB1-treated ducklings.
- Selenium treatment significantly attenuated AFB1-induced mitochondrial DNA mutations, pore opening, and histological liver damage.
Conclusions:
- Selenium demonstrates a potent protective effect against AFB1-induced hepatic mitochondrial damage in ducklings.
- Selenium's protective action may be attributed to its antioxidant properties.
- These findings support selenium's role in mitigating mycotoxin-induced liver injury.
