Due to the increasing use of gold nanoparticles (AuNPs) in different areas such as medicine, biotechnology or food sector, human exposure to them has grown significantly and its toxicity evaluation has become essential. Therefore, the purpose of this study was to compare the potential genotoxic effects of 30, 50 and 90 nm AuNPs, using in vitro comet assay with the in vivo mutagenic and recombinogenic activity (SMART Test) in Drosophila. The results indicated that in both cell lines, 30, 50 and 90 nm (1–10 μg ml⁻¹) AuNPs increased DNA strand breaks following 24 h treatment. This damage was not dose and size-dependent. Moreover, a modified comet assay using endonuclease III and formamidopyrimidine-DNA glycosylase restriction enzymes showed that in both cell lines, pyrimidines and purines were oxidatively damaged by all AuNPs, being 90 nm AuNPs slightly more genotoxic. However, the data obtained with SMART showed that 30 nm AuNPs did not modify the spontaneous frequencies of spots indicating lack of mutagenic and recombinogenic activity. Therefore, further experiments must be carried out to gain a better understanding of the mechanism of action of AuNPs to ensure their safe use.

由于金纳米颗粒（AuNPs）在医学，生物技术或食品领域等不同领域的使用越来越多，因此人们对它们的接触已大大增加，其毒性评估已变得至关重要。因此，本研究的目的是通过使用体外彗星测定与果蝇体内诱变和重组活性（SMART测试）来比较30、50和90 nm AuNPs的潜在遗传毒性作用。结果表明，在两种细胞系中，分别为30、50和90 nm（1–10μgml ^-1）AuNPs在24小时处理后增加了DNA链断裂。这种损害与剂量和大小无关。此外，使用内切核酸酶III和甲酰胺基嘧啶-DNA糖基化酶限制酶的改良彗星试验显示，在两种细胞系中，嘧啶和嘌呤均被所有AuNP氧化损伤，因为90 nm AuNP具有更高的遗传毒性。但是，使用SMART获得的数据表明30 nm AuNPs不会改变斑点的自发频率，表明缺乏诱变和重组活性。因此，必须进行进一步的实验以更好地了解AuNP的作用机理，以确保其安全使用。