Objective: Fluoride toxicity primarily
contributes to the production of reactive oxygen and nitrogen derivatives,
trigger the cell death pathways by causing lipid peroxidation and DNA damage.
Boric acid (BA) contributes to preservation of membrane integrity and function
and maintenance of redox balance due to its high affinity to some metabolites
in the organism. The aim of this study was to investigate the protective effect
of BA on neurodegenerative processes against the toxic effects of sodium
fluoride (NaF) administered at different doses on rat brain synaptosomes.
Material and Methods: Synaptosomes obtained from the
rat frontal cortex were administered at different doses of sodium fluoride (NaF)
to determine the most toxic dose of NaF. Determined toxic dose of NaF for
synaptosomes and BA concentrations were administered in vitro at 37°C for 30min
and then the parameters of malondialdehyde (MDA) level, superoxide dismutase
(SOD) activity, Na/K ATPase activity and DNA fragmentation value were measured
spectrophotometrically.
Results: There was a statistically significant
difference between measured parameters, when the 80mg/L NaF group was compared
with the control group. We found that 10 and 25 mM BA treatment provided a
significant improvement in MDA, SOD, Na/K ATPase and DNA fragmentation compared
to the 80mg/L NaF group. The 5 mM BA concentration was not found effective dose
according to other doses.
Conclusion: In conclusion, BA has potential
for neuroprotective effects against cellular damage caused by NaF. The
results suggest that the BA can be a neuroprotective therapeutic agent for fluoride
toxicity.
Boric acid Neuroprotection Synaptosomes Sodium fluoride Oxidative stress
Birincil Dil | İngilizce |
---|---|
Konular | Sağlık Kurumları Yönetimi |
Bölüm | Araştırma Makalesi |
Yazarlar | |
Yayımlanma Tarihi | 30 Temmuz 2018 |
Yayımlandığı Sayı | Yıl 2018 |