Abstract
Nanoparticles derived from automobile exhaust may tend to travel hundreds of miles from their source of emissions and have an adverse impact on environmental health. Numerous studies have reported that the aquatic environment is known to be a natural recipient of environmental contaminants from the soil and air, which makes aquatic organisms vulnerable to contamination by ultrafine particles/nanoparticles. The present report aimed to investigate the cytogenotoxic potential of sublethal concentrations (0.05 ppm) of diesel and petrol automobile exhaust soot nanoparticles (DAESNPs and PAESNPs) in erythrocytes of the freshwater fish Channa punctatus. Morphological alterations (macrocytes, microcytes, kidney shaped, dacrocytes, notched, burr, sickle shaped and flask shaped), nuclear alterations (bean shaped, notched, lobbed, bud shaped, blebbed and condensed), MNs, oxidative stress, DNA damage and apoptosis were assessed. Increased frequencies of morphological alterations ( average of 7.12 ± 0.71, and 7.24 ± 0.84 in DAESNP- and PAESNP- treated fish, respectively), nuclear alterations ( average of 10.60 ±1.97, and 11.99 ± 1.24 in DAESNP- and PAESNP- treated fish, respectively) and MNs (13.83 ± 0.16, and 11.83 ± 1.58 in DAESNP- and PAESNP- treated fish, respectively) were found. Similarly, compared with that in the control group, the level of malondialdehyde, a byproduct of lipid peroxidation was significantly greater, while the level of reduced glutathione was lower in the DAESNP- and PAESNP- exposed fish. The comet analysis parameters revealed that both DAESNPs and PAESNPs induced DNA damage. In addition, Annexin-V FITC/PI assay data demonstrated that DAESNPs and PAESNPs led to the induction of apoptosis. Our report suggested that morphological and nuclear alterations in the erythrocytes of experimental fish occur in response to genotoxic stress and oxidative stress induced by DAESNPs and PAESNPs. Nonetheless, the apoptosis provoked by DAESNPs and PAESNPs is due to DNA damage.