Antioxidative effect of folate-modified chitosan nanoparticles

Area of Science:

• Biomaterials Science
• Toxicology
• Oxidative Stress Research

Background:

• Nicotine exposure induces significant oxidative stress, leading to tissue injury and compromised antioxidant defense mechanisms.
• Mitochondria and serum are key sites affected by nicotine-induced oxidative damage, impacting cellular function.
• Folate-conjugated carboxymethyl chitosan derivatives show potential for therapeutic intervention against toxic insults.

Purpose of the Study:

• To investigate the protective effects of carboxymethyl chitosan-2, 2' ethylenedioxy bis-ethylamine-folate (CMC-EDBE-FA) against nicotine-induced oxidative stress in mice.
• To evaluate the impact of CMC-EDBE-FA on tissue injury markers, antioxidant status, and glutathione system.
• To assess the compound's efficacy in protecting mitochondria and serum from oxidative damage.

Main Methods:

• CMC-EDBE-FA was synthesized by covalently linking folic acid to carboxymethyl chitosan via 2, 2' ethylenedioxy bis-ethylamine.
• Mice were administered nicotine (1 mg/kg bw/day) and/or CMC-EDBE-FA (1 mg/kg bw/day) for 7 days.
• Key biomarkers including lipid peroxidation, oxidized glutathione, antioxidant enzyme activity, and DNA damage were measured.

Main Results:

• Nicotine administration significantly increased lipid peroxidation, oxidized glutathione levels, and DNA damage compared to controls.
• CMC-EDBE-FA supplementation significantly reduced these markers of oxidative stress and DNA damage.
• The compound effectively ameliorated the reduced antioxidant status observed in nicotine-treated mice, with no adverse effects noted.

Conclusions:

• CMC-EDBE-FA demonstrates significant protective effects against nicotine-induced toxicity.
• The compound is non-toxic and effectively mitigates oxidative stress, tissue injury, and DNA damage.
• CMC-EDBE-FA shows promise as a therapeutic agent for conditions associated with nicotine-induced oxidative damage.