Recent advancements in nanotechnology have led to the exploration of calcium hydroxide nanoparticles (Ca(OH)2NPs) for various applications, particularly due to their potent antimicrobial properties. Yet, little is known about their potential health impacts, especially concerning genomic integrity and apoptosis induction. A new study published in Scientific Reports reveals alarming findings about the effects of Ca(OH)2NPs on human liver cancer cells (HepG2) and normal skin fibroblasts (HSF).
The investigation found significant cytotoxic effects from exposure to Ca(OH)2NPs, with researchers observing concentration-dependent cell death. The study reports IC50 values of 271.93 µg/mL for HSF cells and 291.8 µg/mL for HepG2 cells. This indicates the concentration at which 50% of the cells show reduced viability following treatment.
Crucially, exposure of HepG2 cells to Ca(OH)2NPs not only led to cell death but also induced genomic instability, resulting in DNA damage and triggering oxidative stress within cancer cells. Specifically, treatments at the IC50 concentration led to significant dysregulation of key apoptotic genes, including p53 and Bax (pro-apoptotic markers), and Bcl-2 (an anti-apoptotic factor). This gene dysregulation suggests potential mechanisms through which Ca(OH)2NPs induce apoptosis selectively within cancerous cells.
Interestingly, the same concentration of Ca(OH)2NPs did not exhibit the same genotoxicity or influence on apoptotic gene expression in normal HSF cells. The study emphasizes this selective cytotoxicity, noting, "Exposure to Ca(OH)2NPs at IC50 concentration for 48 h was non-genotoxic in normal HSF cells and selectively disrupts the genomic DNA integrity of HepG2 cancer cells through induction of high DNA damage."
To explore these effects, researchers employed various methodologies, including the Sulforhodamine B (SRB) assay to evaluate cell viability, the alkaline comet assay to assess DNA damage, and qRT-PCR to study the expression levels of apoptosis-related genes. The results indicated alarming levels of reactive oxygen species (ROS) generation, particularly within the HepG2 cells, exacerbated by the nanoparticle exposure. Indeed, the treatment resulted in notable increases of ROS, significantly affecting cellular processes.
The findings prompt urgent attention, as they reveal the potential risks associated with regular human exposure to Ca(OH)2NPs, which could occur through various environmental sources and consumer products. Due to their increasing applications, from biomedicine to construction, the need to evaluate the safety of such nanoparticles is ever more pressing.
Future research is necessary to fully understand the toxicological properties and potential therapeutic roles of Ca(OH)2NPs, particularly focusing on their effectiveness against cancer cells and the safety profile concerning non-cancerous cells. Overall, this study sheds light on the complex interactions of nanoparticles with living cells, underscoring both their potential benefits and risks.