Human exposure to mercury (Hg) is primary associated with its organic form, methylmercury (MeHg), through the ingestion of
contaminated seafood. However, Hg contamination is also positively correlated with the number of dental restorations, total
surface of amalgam, and organic mercury concentration in the saliva. Among the cells existing in the oral cavity, human
periodontal ligament fibroblast (hPLF) cells are important cells responsible for the production of matrix and extracellular
collagen, besides sustentation, renewal, repair, and tissue regeneration. In this way, the present study is aimed at investigating
the potential oxidative effects caused by MeHg on hPLF. Firstly, we analyzed the cytotoxic effects of MeHg (general
metabolism status, cell viability, and mercury accumulation) followed by the parameters related to oxidative stress (total
antioxidant capacity, GSH levels, and DNA damage). Our results demonstrated that MeHg toxicity increased in accordance
with the rise of MeHg concentration in the exposure solutions (1-7 ?M) causing 100% of cell death at 7 ?M MeHg exposure.
The general metabolism status was firstly affected by 2 ?M MeHg exposure (43:8?1:7%), while a significant decrease of cell
viability has arisen significantly only at 3 ?M MeHg exposure (68:7?1:4%). The ratio among these two analyses (named fold
change) demonstrated viable hPLF with compromised cellular machinery along with the range of MeHg exposure.
Subsequently, two distinct MeHg concentrations (0.3 and 3 ?M) were chosen based on LC50 value (4.2 ?M). hPLF exposed to
these two MeHg concentrations showed an intracellular Hg accumulation as a linear-type saturation curve indicating that
metal accumulated diffusively in the cells, typical for metal organic forms such as methyl. The levels of total GSH decreased
50% at exposure to 3 ?M MeHg when compared to control. Finally, no alteration in the DNA integrity was observed at
0.3 ?M MeHg exposure, but 3 ?M MeHg caused significant damage. In conclusion, it was observed that MeHg exposure
affected the general metabolism status of hPLF with no necessary decrease on the cell death. Additionally, although the
oxidative imbalance in the hPLF was confirmed only at 3 ?M MeHg through the increase of total GSH level and DNA
damage, the lower concentration of MeHg used (0.3 ?M) requires attention since the intracellular mercury accumulation may
be toxic at chronic exposures.
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