As an important part of artificial nanomaterials, carbonaceous nanomaterials (CNMs) are widely applied in a plenty of areas such as energy, manufacturing and pharmaceutical industries. In the present study, the developmental toxicity, induced by three typical CNMs including graphene oxide (GO), carbon nanotube (CNT) and graphene oxide quantum dot (GOQD) was investigated in the typical model animal, zebrafish larva. The induced sub-acute toxicity at the low concentration of GO, CNT and GOQD was investigated in adult zebrafish, either. Moreover, the molecular mechanisms at the level of metabolomics were also explored. The results showed that there was a significant increase in reactive oxygen species (ROS), and mitochondrial membrane damage was caused by GO, CNT and GOQD in zebrafish larva. However, there was no significant developmental toxicity on zebrafish larva. The toxicity order in terms of the ROS increase and mitochondrial membrane damage was GOQD > CNT > GO. The chronic exposure at the typical environment-associated concentration (0.01 mg·L-1) of CNMs can induce gill and kidney cell senescence of adult zebrafish. Meanwhile, it can also inhibit total superoxide dismutase (T-SOD) activity in adult zebrafish in the subacute toxicity test (21 d) at the concentration of 0.01 mg·L-1. The metabolomics research revealed that the toxicity order at the environment-associated concentration acting on adult zebrafish was GOQD > CNT > GO; and it showed that fatty acids and proline turbulence may be responsible for one of the molecular mechanisms of T-SOD inhibition in adult zebrafish. This work can supply rationale to evaluate the potential risk of ecosystems and human health induced by the three typical CNMs.