Antioxidants, Oxidative Stress, and Non-Communicable Diseases

Crisóstomo, Luís; Oliveira, Pedro F.; Alves, Marco G.

doi:10.3390/antiox11061080

Cited by 5 publications

(1 citation statement)

References 11 publications

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“…The primary consequence of oxidative stress is damage to biological macromolecules, including nucleic acids, proteins, and fats, leading to oxidation, hydrolysis, and methylation of DNA, as well as the accumulation of unfolded proteins and lipid oxidation products [1,4]. The onset of multiple chronic diseases such as diabetes and its complications, hypertension, atherosclerosis, tumors, kidney damage, and neurodegenerative disease are significantly influenced by these impairments [5][6][7][8]. The aging process of the organism is also a major contributor to many chronic disorders [9].…”

Section: Introductionmentioning

confidence: 99%

The Potential of Bioactive Fish Collagen Oligopeptides against Hydrogen Peroxide-Induced NIH/3T3 and HUVEC Damage: The Involvement of the Mitochondria

Zhu,

Liu,

et al. 2024

Nutrients

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Extensive in vivo investigations have demonstrated the antioxidant properties of fish collagen oligopeptides (FCOPs). One of the main causes of aging and chronic non-communicable diseases is oxidative stress. Therefore, FCOPs have a broad range of applications in illness prevention and delaying aging from the standpoint of the “food is medicine” theory. However, the mechanisms that underpin the antioxidant activity of FCOPs are not completely understood. The specific objective of this essay was to investigate the antioxidant effect of FCOPs and its possible mechanism at the cellular level. Mouse embryonic fibroblasts NIH/3T3 and human vein endothelial cells (HUVECs) were exposed to 200 µM hydrogen peroxide containing different concentrations of FCOPs for 4 h and were supplemented with different concentrations of FCOPs for 24 h. Normal growth medium without FCOPs was applied for control cells. An array of assays was used to evaluate the implications of FCOPs on cellular oxidative stress status, cellular homeostasis, inflammatory levels, and mitochondrial function. We found that FCOPs exerted a protective effect by inhibiting reactive oxygen species (ROS) production, enhancing superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS) activities and cell viability, inhibiting cell cycle arrest in the G1 phase, suppressing interleukin-1β (IL-1β), IL-6, matrix metalloproteinase-3 (MMP-3) and intercellular adhesion molecule-1(ICAM-1) secretion, downregulating nuclear factor-kappa B (NF-κB) activity, protecting mitochondrial membrane potential, and increasing ATP synthesis and NAD+ activities in both cells. FCOPs had a stronger antioxidant impact on NIH/3T3 than on HUVECs, simultaneously increasing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) content in NIH/3T3. These findings indicate that FCOPs have antioxidant effects on different tissue cells damaged by oxidative stress. FCOPs were therefore found to promote cellular homeostasis, inhibit inflammation, and protect mitochondria. Meanwhile, better health outcomes will be achieved by thoroughly investigating the effective dose and intervention time of FCOPs, as the absorption efficiency of FCOPs varies in different tissue cells.

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