ArticleACS omega2026
Spermidine Supplementation Reduces Genetic Damage in the Liver and Bone Marrow of Rodents.
Article in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
Funding
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Abstract
Mutations in DNA constitute the initial step in the process of carcinogenesis. While diets high in sugar increase the risk of various diseases, a balanced diet rich in bioactive compounds can mitigate DNA damage. Spermidine (SPD) is a polyamine with reported effects on autophagy induction, inflammation reduction, and the enhancement of immune function. Within this context, we investigated the effects of SPD supplementation [10 and 30 mg/kg body weight (bw)] in male Swiss mice over a period of 44 days. The animals were divided into two groups: one fed a standard diet (SDNuvilab CR1), and the other fed a standard diet enriched with 30% sucrose (SU) (SDSU). On day 44, the mutagenic agent methylmethanesulfonate [MMS 40 mg/kg bw intraperitoneal (ip)] was administered to induce mutagenicity. On day 45, bone marrow and liver cell samples were collected to evaluate the chemopreventive potential and oxidative stress. The results showed that SDSU significantly reduced feed intake and increased water consumption. None of the treatments exhibited cytotoxic or mutagenic effects. Animals treated with SPD 30 mg/kg bw combined with MMS, under both SD and SDSU conditions, showed a reduction in the frequency of micronucleated polychromatic erythrocytes (MNPCEs) in bone marrow and reduced DNA damage in liver cells, particularly when they were not associated with SU consumption. Additionally, significantly increased catalase (CAT) and superoxide dismutase (SOD) levels were observed, suggesting that the genoprotective effect against induced damage may be at least partially related to mobilization of the endogenous antioxidant defense system.
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Registered trials
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