RESUMO
This study aimed to investigate the toxicity and endocrine disrupting potential of a complex mixture of polycyclic aromatic hydrocarbons (PAHs) in the estrogen pathway using hepatocytes of Nile tilapia Oreochromis niloticus, the hepatocytes were exposed to various concentrations of the PAH mixture, and multiple endpoints were evaluated to assess their effects on cell viability, gene expression, oxidative stress markers, and efflux activity. The results revealed that the PAH mixture had limited effects on hepatocyte metabolism and cell adhesion, as indicated by the non-significant changes observed in MTT metabolism, neutral red retention, and crystal violet staining. However, significant alterations were observed in the expression of genes related to the estrogen pathway. Specifically, vitellogenin (vtg) exhibited a substantial increase of approximately 120% compared to the control group. Similarly, estrogen receptor 2 (esr2) showed a significant upregulation of approximately 90%. In contrast, no significant differences were observed in the expression of estrogen receptor 1 (esr1) and the G protein-coupled estrogen receptor 1 (gper1). Furthermore, the PAH mixture elicited complex responses in oxidative stress markers. While reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels remained unchanged, the activity of catalase (Cat) was significantly reduced, whereas superoxide dismutase (Sod) activity, glutathione S-transferase (Gst) activity, and non-protein thiols levels were significantly elevated. In addition, the PAH mixture significantly influenced efflux activity, as evidenced by the increased efflux of rhodamine and calcein, indicating alterations in multixenobiotic resistance (MXR)-associated proteins. Overall, these findings, associated with bioinformatic analysis, highlight the potential of the PAH mixture to modulate the estrogen pathway and induce oxidative stress in O. niloticus hepatocytes. Understanding the mechanisms underlying these effects is crucial for assessing the ecological risks of PAH exposure and developing appropriate strategies to mitigate their adverse impacts on aquatic organisms.
RESUMO
The effects of clastogenic or mutagenic agents have rarely been studied in neotropical fish species exposed to contaminated water. In this study, the genetic damage caused by lead in the widely distributed South American fish, Hoplias malabaricus, was assessed using the comet (SCGE) assay and by testing for chromosomal aberrations. Eighteen specimens were acclimatized to laboratory conditions and then chronically exposed to contaminated food by feeding prey (Cyprinus sp.) injected intraperitoneally with doses of inorganic lead adjusted to give a contamination level of 21 mg of Pb2+.g-1 net weight of H. malabaricus. Three fish were sampled for chromosomal analysis after four doses (18 days) and another three after eight doses (41 days) of lead and the results then compared with three untreated controls kept under lead-free conditions. An additional six treated fish and three controls were sampled for the comet assay after 13 doses (64 days). Exposure to lead significantly increased the frequency of chromosomal aberrations and the frequency of tailed cell nuclei, the latter indicating DNA damage. These results show that H. malabaricus is a useful biological model for screening the clastogenic effects of lead and possibly other xenobiotics. The genetic damage seen here illustrates the need to investigate the potential effects of heavy metals on fish species in South America.