Spermidine Supplementation Reduces Genetic Damage in the Liver and Bone Marrow of Rodents

TL;DR

Spermidine supplementation in mice reduced DNA damage in the liver and bone marrow, especially when combined with a mutagen.

Contribution

The study shows spermidine's genoprotective effects in rodents under different dietary conditions.

Findings

Spermidine reduced micronucleated polychromatic erythrocytes in bone marrow.

Spermidine lowered DNA damage in liver cells, particularly without sucrose.

Antioxidant enzyme levels (CAT and SOD) increased with spermidine treatment.

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 (SDNuvilab 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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