The Protective Effect of Zinc Supplementation Against Oxidative Stress and Oxidative Modifications of Cellular...

In a rat model simulating moderate and relatively high human exposure to cadmium (Cd; 5 and 50 mg/L, respectively, for 12 months), it was examined whether zinc (Zn) supplementation (30 and 60 mg/L, increasing the daily intake of this element by 71% and 146%, respectively) could protect against this xenobiotic-caused disruption of the oxidative-reductive balance in the mandibular bone tissue and the subsequent oxidative damage to nucleic acids, proteins, and lipids. The exposure to Cd weakened the enzymatic antioxidative barrier (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)) and decreased the total antioxidative status (TAS) of this tissue. The treatment with Cd also increased the concentration of hydrogen peroxide (H₂O₂) and the total oxidative status (TOS) of the mandibular bone tissue, leading to the development of oxidative stress, as indicated by an elevated value of the oxidative stress index (OSI), and oxidative damage to nucleic acids, lipids, and proteins. Zn supplementation at 30 and 60 mg/L during Cd exposure at 5 and 50 mg/L effectively protected against the accumulation of this toxic heavy metal in mandibular bone tissue and prevented oxidative stress and oxidative modifications of nucleic acids, proteins, and lipids. In conclusion, increasing Zn intake by at least 71% during chronic oral exposure to Cd may prevent oxidative-antioxidative imbalance and the development of oxidative stress, thereby safeguarding cellular macromolecules in the mandibular bone tissue from oxidative damage. These findings highlight the potential role of Cd exposure in the aetiology of mandibular bone damage and provide the first evidence that Zn supplementation may represent an effective intervention to alleviate adverse impact of long-term oral exposure to Cd on mandibular bone.