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Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)
Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)
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Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)
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Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)
Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)

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Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)
Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)
Journal Article

Diesel Particulate Matter (DPM)-Induced Metabolic Disruption in Mice Is Mitigated by Sodium Copper Chlorophyllin (SCC)

2025
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Overview
Background/Objectives: The increasing prevalence of metabolic disorders underscores the need for effective interventions to mitigate environmental stressors such as diesel particulate matter (DPM), a major urban air pollutant. DPM is composed of fine carbonaceous particles that can induce systemic inflammation. This phenomenon results in metabolic dysfunction such as adipocyte hypertrophy, insulin resistance, and mitochondrial impairment in body tissues. Methods: This study investigated the impact of DPM exposure on murine lung, skeletal muscle, and adipose tissues and evaluated the protective effects of supplementation with sodium copper chlorophyllin (SCC). Results: Compared to controls, DPM-exposed mice exhibited significantly elevated oxidative stress markers (* p ≤ 0.05), systemic pro-inflammatory cytokines including TNF-α, MCP-1, IL-6, and IL-1β (* p ≤ 0.05), and adipocyte hypertrophy of both subcutaneous and visceral fat depots, supporting prior findings of DPM-induced metabolic dysfunction. SCC supplementation restored pulmonary ATP levels (* p ≤ 0.05), significantly reduced ROS production in lung and muscle tissue (* p ≤ 0.05), and significantly attenuated DPM-induced inflammatory cytokine secretion (* p ≤ 0.05), while lessening DPM-induced adipocyte hypertrophy. Conclusions: These effects highlight the antioxidant and anti-inflammatory potential of SCC, which likely mitigates systemic metabolic compromise by modulating mitochondrial function and inflammatory pathways. This study further demonstrated that SCC supplementation may be an effective intervention for alleviating the adverse effects of DPM exposure on metabolic and inflammatory compromise. Additional research may clarify a role for SCC in reducing systemic health risks associated with air pollution and offer a foundation for future translational research in human populations exposed to environmental pollutants.