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Selenium antagonizes cadmium-induced apoptosis in chicken spleen but not involving Nrf2-regulated antioxidant
Menghao Chen1, Xiaojing Li1, Ruifeng Fan1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
Abstract:
The nuclear transcription factor NF-E2-related factor 2 (Nrf2) binds to antioxidant response elements (AREs) and is involved in the regulation of genes participated in defending cells against oxidative damage, which have been confirmed in animal models. Selenium (Se), known as an important element in the regulation of antioxidant activity, can antagonize Cadmium (Cd) toxicity in birds. However, the role of Nrf2 in selenium-cadmium interaction has not been reported in birds. To further explore the mechanism of selenium attenuating spleen toxicity induced by cadmium in chickens, cadmium chloride (CdCl2, 150mg/kg) and sodium selenite (Na2SeO3, 2mg/kg) were co-administrated or individually administered in the diet of chickens for 90 days. The results showed that Cd exposure increased the level of hydrogen peroxide (H2O2) and malondialdehyde (MDA) and decreased the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (Gpx), total antioxidative capacity (T-AOC), catalase (CAT). Cd exposure increased obviously nuclear accumulation of Nrf2, and the expression of Nrf2 downstream heme oxygenase-1 (HO-1) and NAD(P)H: quinine oxidoreductase 1 (NQO1), reduced the expression of Kelch-like ECH-associated protein (keap1), Gpx-1 and thioredoxin reductase-1 (TrxR1). In addition, Cd induced the increase of bak, caspase9, p53, Cyt c mRNA levels, increased bax/bcl-2 ratio, increased caspase3 mRNA and protein levels. Selenium treatment reduced the accumulation of Cd in the spleen, attenuates Cd-induced Nrf2 nuclear accumulation, enhanced antioxidant enzyme activities, ameliorated Cd-induced oxidative stress and apoptosis in the spleen. In summary, our results demonstrate that Se ameliorated spleen toxicity induced by cadmium by modulating the antioxidant system, independently of Nrf2-regulated antioxidant response pathway.
Insights
Selenium (Se) mitigates cadmium (Cd) spleen toxicity in chickens by enhancing the antioxidant system. This protective effect occurs independently of the Nrf2-regulated antioxidant response pathway, suggesting a distinct mechanism of action for Se.
Area of Science:
- Environmental Toxicology
- Nutritional Biochemistry
- Avian Physiology
Background:
- Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates antioxidant genes involved in cellular defense against oxidative damage.
- Selenium (Se) is known to counteract cadmium (Cd) toxicity, particularly in avian species.
- The specific role of Nrf2 in the interaction between Se and Cd toxicity in birds remains unelucidated.
Purpose of the Study:
- To investigate the mechanism by which selenium attenuates cadmium-induced spleen toxicity in chickens.
- To determine the involvement of the Nrf2-regulated antioxidant response pathway in the protective effects of selenium against cadmium toxicity.
Main Methods:
- Chickens were administered cadmium chloride (CdCl2) and sodium selenite (Na2SeO3) individually or concurrently via diet for 90 days.
- Assessed oxidative stress markers (H2O2, MDA), antioxidant enzyme activities (SOD, Gpx, T-AOC, CAT), and apoptosis-related factors (bak, caspase9, p53, Cyt c, bax/bcl-2, caspase3).
- Quantified Nrf2 nuclear accumulation and the expression of its downstream targets (HO-1, NQO1) and regulators (keap1, Gpx-1, TrxR1).
Main Results:
- Cadmium exposure increased oxidative stress and apoptosis in the spleen, alongside elevated Nrf2 nuclear accumulation and specific downstream gene expression.
- Selenium treatment reduced cadmium accumulation in the spleen, enhanced antioxidant enzyme activities, and ameliorated Cd-induced oxidative stress and apoptosis.
- Selenium's protective effects were observed despite a reduction in Cd-induced Nrf2 nuclear accumulation, indicating an Nrf2-independent mechanism.
Conclusions:
- Selenium effectively ameliorates cadmium-induced spleen toxicity in chickens by modulating the antioxidant system.
- The protective mechanism of selenium against cadmium toxicity in the spleen operates independently of the Nrf2-regulated antioxidant response pathway.
- These findings highlight a distinct pathway through which selenium exerts its protective effects against heavy metal toxicity in avian species.