This experimental analysis reveals how persistent organic pollutants and hydrogen peroxide significantly affect oxidative stress in Wistar rats, suggesting the need for antioxidant strategies.
Persistent organic pollutants (POPs) and oxidative stress are key contributors to cellular dysfunction and disease progression. This study investigates the synergistic effects of POPs, specifically benzo(a)pyrene and naphthalene, in combination with hydrogen peroxide (H₂ O₂ ) on oxidative stress markers in a comparative experimental model with two treatment durations: Batch 1 (4 weeks) and Batch 2 (8 weeks). Biochemical assessments included superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malondialdehyde (MDA), and glutathione peroxidase (GPx). The results revealed significant oxidative stress in groups exposed to POPs alone, with MDA levels increasing from 2.70 ± 0.28 (control) to 6.40 ± 0.14 in Batch 1 and from 2.60 ± 0.42 to 9.45 ± 0.35 in Batch 2, indicating progressive lipid peroxidation. This was accompanied by a decline in GSH levels (3.35 ± 0.21 to 2.35 ± 0.21 in Batch 2), SOD (18.20 ± 0.28 to 10.40 ± 0.14 in Batch 2), and CAT (17.20 ± 0.28 to 12.65 ± 0.21 in Batch 2), confirming oxidative stress-induced depletion of antioxidant defenses. Exposure to H₂ O₂ alone exacerbated oxidative damage, with MDA levels reaching 8.30 ± 0.42 in Batch 1 and 10.30 ± 0.28 in Batch 2, along with a significant reduction in GSH (2.35 ± 0.21 in Batch 2). Co-exposure to POPs and low-dose H₂ O₂ resulted in moderate oxidative stress, as seen in MDA levels of 9.20 ± 0.28 (Batch 1) and 12.50 ± 0.28 (Batch 2). High-dose H₂ O₂ combined with POPs induced severe oxidative damage, with the highest MDA levels (10.30 ± 0.28 in Batch 1 and 14.35 ± 0.21 in Batch 2) and a sharp depletion in GSH (1.10 ± 0.14 in Batch 2). Vitamin C supplementation provided partial protection, lowering MDA levels to 4.45 ± 0.35 (Batch 1) and 3.60 ± 0.28 (Batch 2), while restoring some antioxidant enzyme activities, particularly SOD and GPx. However, its effectiveness diminished in Batch 2, indicating that prolonged oxidative stress may reduce antioxidant efficacy. These findings highlight a dose- and duration-dependent synergistic effect between POPs and H₂ O₂ , with protracted exposure exacerbating oxidative damage. The study emphasizes the potential risks associated with combined environmental toxicants and oxidative stressors in inducing cellular damage and the need for effective antioxidant interventions.
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Amadi et al. (2025) studied this question.
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