Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
Esculin mitigates nickel chloride-induced generation of ROS, hemoglobin oxidation, and alterations in redox status in human red blood cells.
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Sharma Monika, Khan Fahim Halim, Mahmood Riaz
Аннотация
BACKGROUND: Nickel (Ni) is a heavy metal and an environmental pollutant that is harmful to humans because of its carcinogenicity and toxic effects on several tissues and organs. Due to their widespread use concerns have been raised about the potential adverse effects of Ni and its compounds on human health. Ni compounds induce oxidative stress in cells by modifying the redox equilibrium. This work studied the protective role of the plant antioxidant esculin (ES) against nickel chloride (NiCl2)-induced oxidative damage and cytotoxicity in isolated human red blood cells (RBC).
METHODS: Human RBC were first incubated with varying concentrations of ES (0.25-1.0 mM) for 2 h at 37 °C, followed by addition of 0.5 mM NiCl2 and further incubation for 24 h at 37 °C.
RESULTS: Treatment of RBC with NiCl2 alone increased the production of reactive oxygen species and significantly enhanced methemoglobin level, heme degradation, free iron release and hydrogen peroxide content. It also led to oxidation of cellular thiol groups, proteins and lipids. The glutathione content, total sulfhydryl groups, nitric oxide level and free amino groups were decreased. The activities of antioxidant, metabolic and plasma membrane enzymes were inhibited and the antioxidant capacity of RBC was lowered. However, pre-incubation of RBC with ES greatly mitigated the NiCl2-induced alterations in these parameters in an ES concentration-dependent manner. In all cases ES alone did not exhibit any significant toxic effect. This was confirmed by electron microscopic analysis of RBC. Treatment with NiCl2 alone resulted in the conversion of biconcave discoidal RBC to echinocytes but this change in cell morphology was greatly prevented in the presence of ES. The ES alone treated RBC did not show altered cell morphology.
CONCLUSION: These results suggest that ES can be potentially used as a cytoprotectant against Ni-induced toxicity.
METHODS: Human RBC were first incubated with varying concentrations of ES (0.25-1.0 mM) for 2 h at 37 °C, followed by addition of 0.5 mM NiCl2 and further incubation for 24 h at 37 °C.
RESULTS: Treatment of RBC with NiCl2 alone increased the production of reactive oxygen species and significantly enhanced methemoglobin level, heme degradation, free iron release and hydrogen peroxide content. It also led to oxidation of cellular thiol groups, proteins and lipids. The glutathione content, total sulfhydryl groups, nitric oxide level and free amino groups were decreased. The activities of antioxidant, metabolic and plasma membrane enzymes were inhibited and the antioxidant capacity of RBC was lowered. However, pre-incubation of RBC with ES greatly mitigated the NiCl2-induced alterations in these parameters in an ES concentration-dependent manner. In all cases ES alone did not exhibit any significant toxic effect. This was confirmed by electron microscopic analysis of RBC. Treatment with NiCl2 alone resulted in the conversion of biconcave discoidal RBC to echinocytes but this change in cell morphology was greatly prevented in the presence of ES. The ES alone treated RBC did not show altered cell morphology.
CONCLUSION: These results suggest that ES can be potentially used as a cytoprotectant against Ni-induced toxicity.