ERYTHROCYTE MEMBRANE-STABILITY AND PROPHYLACTIC POTENTIALS OF CHRYSIN AND RUTIN ON TRICHLOROETHYLENE-ENGENDERED ERYTHROCYTOTOXICITY IN WISTAR RATS
Keywords:
Trichloroethylene, rutin, chrysin, erythrocytes, antioxidants, dyslipidemiaAbstract
Trichloroethylene (TCE) is a halogenated alkene solvent linked to several cancers and autoimmune diseases in humans and animals and is a contaminant of the air, water, and soil. Chrysin and rutin are known to modulate oxidants, antioxidants, and lipotoxicity. However, their mechanistic effect on TCE-prompted red blood cell injury remains undetermined. This investigation hypothesized that chrysin and rutin could offer an alleviative influence on TCE-triggered erythrocyte damage. Randomization was employed to earmark forty-eight rats into eight groups (6 rats/group): control, chrysin and/or rutin (100 mg.kg⁻¹ day⁻¹), TCE only (1,000 mg.kg⁻¹day⁻¹), chrysin and/or rutin (100 mg.kg⁻¹day⁻¹) treated with TCE. Rats were pre-treated orally by gavage with flavonoid therapy (chrysin and/or rutin) every day for fourteen days before administering a single dosage of TCE. Twenty-four hours following TCE administration, the rats were euthanized, and their blood was taken for biochemical assays. Chrysin and/or rutin pretreatment pronouncedly (p < 0.05) mitigated TCE-engendered increases in lipids (triacylglycerol and cholesterol) concentrations, reactive oxygen/nitrogen specie (NO) levels, lipid peroxidation (MDA) amounts, and myeloperoxidase activity. The two flavonoids equally attenuated TCE-invoked depletions in haemoglobin, haematocrit, and total thiol levels, antioxidant enzymes (glutathione-S-transferase, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase), and lactate dehydrogenase (LDH). Improved antioxidant status, and activities of LDH in rats pretreated with the therapeutic agents are indicators of the membrane stability potential of the agents against the cellular assaults of TCE. Therefore, this study suggests that chrysin and/or rutin pretreatment abated TCE-provoked erythrocytes perturbations in rats possibly via radical trapping, antioxidants augmentation, anti-dyslipidemic mechanisms and positive modulation of LDH activity.
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