Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2026
Evaluation of the protective effects of selenium against iron overload-induced toxicity in rats using a multiple-markers approach.
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Ghayth Alzwawy Ateeqah, Khazri Abdelhafidh, Kouki Ahmed, Ben Ali Manel, Ben-Attia Mossadok, Mahmoudi Ezzeddine, Sakly Mohsen, Sellami Badreddine
Аннотация
BACKGROUND: Iron overload can promote the generation of reactive oxygen species (ROS), leading to oxidative stress and different human diseases. The trace element selenium has biological functions and can act as both an antioxidant and a prooxidant. This study aimed to evaluate the protective effects of selenium against iron overload-induced toxicity in rats. Adult Wistar rats were exposed to three increasing concentrations of iron (25, 50, and 100 mg/kg body weight [b.w.]), either alone or in combination with selenium (0.5 mg/kg b.w.).
METHODS: The biological interactions between these two compounds were investigated at the biochemical level in the liver, spleen, kidney, and pancreas.
RESULTS: Our results indicated that iron used alone induces oxidative stress. In all tissues studied and at all the administered doses, we observed changes in the levels of catalase (CAT), glutathione (GSH), glutathione-S-transferase (GST), malondialdehyde (MDA), and acetylcholinesterase (AChE). The responses were dose- and organ-dependent. Selenium administered at 0.5 mg/kg b.w. attenuate the adverse effects of the different iron dosages.
CONCLUSION: These findings highlight the potential application of selenium in mitigating oxidative stress and organ toxicity associated with iron overload. Our research carries significant implications for the development of nutritional and therapeutic strategies aimed at managing disorders related to iron metabolism.
METHODS: The biological interactions between these two compounds were investigated at the biochemical level in the liver, spleen, kidney, and pancreas.
RESULTS: Our results indicated that iron used alone induces oxidative stress. In all tissues studied and at all the administered doses, we observed changes in the levels of catalase (CAT), glutathione (GSH), glutathione-S-transferase (GST), malondialdehyde (MDA), and acetylcholinesterase (AChE). The responses were dose- and organ-dependent. Selenium administered at 0.5 mg/kg b.w. attenuate the adverse effects of the different iron dosages.
CONCLUSION: These findings highlight the potential application of selenium in mitigating oxidative stress and organ toxicity associated with iron overload. Our research carries significant implications for the development of nutritional and therapeutic strategies aimed at managing disorders related to iron metabolism.