Carbonyl reducing enzymes play important roles in the Phase I metabolism of many carbonyl group bearing xenobiotics (Fig. 1) [1,2]. On the other hand, these enzymes metabolize endogenous signal molecules such as steroid hormones, prostaglandines, biogenic amines, as well as sugars and lipid peroxidation derived carbonyls, and are therefore involved in the (patho)physiology of frequent diseases including diabetes, hypertension, the metabolic syndrome, osteoporosis, cancer and neurodegenerative disorders (Fig. 2)[3]. The importance of carbonyl reduction could be demonstrated in the model organism Drosophila melanogaster, where the carbonyl reductase „sniffer“ protects against age-dependent neurodegeneration [4,5]. The enzyme „sniffer“, a homodimeric carbonyl reductase that belongs to the shortchain dehydrogenase/reductase (SDR) superfamily, shares identity to the human enzyme carbonyl reductase type I (CBR1) [6,7]. „Sniffer“ is also common in other species like Daphnia, which are classical organisms for aquatic toxicity testing. Recently, the carbonyl reductase “sniffer” has been identified in the Blue mussel Mytilus spp. (Fig. 3). Millions of tonnes of munitions that have been dumped after World War II pose a new threat to the seas worldwide, since the metal vessels corrode and the toxic explosives trinitrotoluene (TNT) and metabolites leak into the environment [8,9]. Therefore, specific biomarkers are urgently sought to detect TNT contaminations and to perform a risk assessment both for the ecosphere and the human sea food consumer. In the present study, we provide evidence that TNT induces gene expression of the carbonyl reductase „sniffer“ in blue mussels.