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Published on: July 3, 2015
Spermidine Supplementation Reduces Genetic Damage in the Liver and Bone Marrow of Rodents
Janine Barcelos Chacon1,2, Maria Clara Duarte2, Michele Oliveira Carvalho2
1Programa de Pós-graduação em Nutrição e Longevidade, Universidade Federal de Alfenas Alfenas, UNIFAL, Rua Gabriel Monteiro da Silva, 700, Centro, Alfenas, Minas Gerais 37130-001, Brasil.
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.
Insights
Spermidine (SPD) supplementation reduced DNA damage in mice, particularly when combined with a standard diet. This genoprotective effect may stem from enhanced antioxidant defenses, suggesting SPD
Area of Science:
- Biochemistry and Molecular Biology
- Toxicology
- Nutritional Science
Background:
- DNA mutations are the first step in carcinogenesis.
- High-sugar diets increase disease risk, while bioactive compounds can mitigate DNA damage.
- Spermidine (SPD) is a polyamine known for autophagy induction, inflammation reduction, and immune function enhancement.
Purpose of the Study:
- To investigate the chemopreventive potential of spermidine (SPD) supplementation against mutagenicity induced by methylmethanesulfonate (MMS).
- To evaluate the effects of SPD on oxidative stress markers in mice fed standard or high-sucrose diets.
Main Methods:
- Male Swiss mice were fed either a standard diet (SD) or a high-sucrose diet (SDSU) for 44 days.
- Mice received methylmethanesulfonate (MMS) to induce mutagenicity.
- Bone marrow and liver cells were analyzed for DNA damage (micronucleated polychromatic erythrocytes) and oxidative stress markers (catalase, superoxide dismutase).
Main Results:
- Spermidine (SPD) supplementation at 30 mg/kg body weight reduced DNA damage in bone marrow and liver cells following MMS administration.
- The protective effect of SPD was more pronounced in mice on a standard diet compared to those on a high-sucrose diet.
- SPD treatment led to increased levels of antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD).
Conclusions:
- Spermidine (SPD) exhibits genoprotective effects against MMS-induced DNA damage in mice.
- The antioxidant defense system, involving CAT and SOD, plays a role in SPD's protective mechanism.
- Dietary context, specifically high sucrose intake, may influence the efficacy of spermidine's protective effects.

