Asia Pacific Journal of Medical Toxicology (Sep 2024)

Japanese Sake Yeast Potentially Attenuates Arsenic Neurotoxicity in Male Rats Model: Behavioral, Oxidative Stress, and Immunogenetics Assessment

  • Sadaf Saeedi,
  • Ali Olfati,
  • Tayebeh Sadeghi,
  • Firoozeh Veisi,
  • Maryam Zanganeh,
  • Nasrin Jalilian,
  • Sareh Farshadfar,
  • Samad Nazemi,
  • Hamed Khorami

DOI
https://doi.org/10.22038/apjmt.2024.82894.1475
Journal volume & issue
Vol. 13, no. 3
pp. 84 – 89

Abstract

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Background: Arsenic (AS) is widely distributed in our surroundings, causing various health problems like neurological disorders. The current research was designed to investigate the effect of the anti-oxidant and anti-inflammatory content of sake yeast on the recovery of brain damage in an AS-treated rat's model with behavioral, oxidative stress, and immunogenetics assessment.Method: Twenty-four male rats were treated with AS (3 mg/kg b.wt. per day) alone or in combination form with sake (45 mg/kg b.wt. per day), and animals received them for 30 days in drinking water (n=6/group). The initial mechanism of action was explored by behavioral tests (rotarod, amphetamine rotation, and spatial memory(, oxidative assay, and histopathology methods.Results: Considering the vehicle group, induction of brain abnormalities by AS significantly (P<0.05) decreased the number of substantia nigra neurons, total antioxidant capacity, glutathione peroxidase activity and increased the amount of α-synuclein protein and led to the massive accumulation of malondialdehyde. Meanwhile, sake supplementation can rescue the brain damage caused by this toxic metal, resulting in a reduction of malondialdehyde and α-synuclein protein levels, plus a considerable improvement in blood serum total antioxidant capacity consideration (P<0.05). Activity behavioral tests confirmed the AS-mentioned changes by increasing the number of rotations and rod test time. Histopathology assays mimic the above data.Conclusion: In sum, the sake yeast supplement due to its properties positively influences for improvement of dopaminergic neuron dysfunction via AS damage.

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