Biochemical biomarker responses of green-lipped mussel, Perna canaliculus, to acute and subchronic waterborne cadmium toxicity

• Published in: Aquatic toxicology 2013-09, Vol.140-141, p.303-313
• Main Authors: Chandurvelan, Rathishri, Marsden, Islay D., Gaw, Sally, Glover, Chris N.
• Format: Article
• Language: English
• Subjects: acute exposure; alkaline phosphatase; Alkaline Phosphatase - metabolism; Animals; biomarkers; Biomarkers - metabolism; Cadmium; Cadmium - metabolism; Cadmium - toxicity; catalase; Catalase - metabolism; energy; Environmental Exposure; Enzyme Activation - drug effects; Enzyme biomarkers; Gills - drug effects; Glycogen; Glycogen - metabolism; hemolymph; homeostasis; indicator species; lipid peroxidation; Lipid Peroxidation - drug effects; Metallothionein - metabolism; Metallothionein-like protein; mussels; Oxidative stress; Perna - drug effects; Perna - metabolism; Perna canaliculus; pollution; seawater; Time Factors; toxicity; Water Pollutants, Chemical - toxicity
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/j.aquatox.2013.06.015

•Biochemical biomarkers were measured to assess effects of Cd on Perna canaliculus.•Biochemical responses varied between acute and subchronic exposure to Cd.•MTLP induction correlated strongly with Cd accumulation.•Alkaline phosphatase and glycogen levels decreased during subchronic Cd exposure.•Duration of Cd exposure influenced biochemical biomarker responses in mussels. The biochemical responses of the green-lipped mussel, Perna canaliculus, to waterborne cadmium (Cd) were investigated in order to delineate toxic mechanisms, and the impacts of exposure dose and duration, of this important toxicant in a potential sentinel species. Mussels were exposed for either 96h (acute: 0, 2000, 4000μgL−1 Cd) or for 28d (subchronic: 0, 200, 2000μgL−1 Cd), and the digestive gland, gill and haemolymph were examined for impacts. Biochemical responses measured included those associated with metal detoxification (metallothionein-like protein; MTLP), oxidative stress (catalase, lipid peroxidation), cellular homeostasis (alkaline phosphatase, Na+, K+-ATPase; NKA), and energy utilisation (glycogen, haemolymph protein). Following acute exposure, digestive gland glycogen and gill NKA activity were significantly altered by Cd exposure relative to levels in mussels exposed to Cd-free seawater. Subchronic Cd exposure resulted in a significant increase in MTLP levels in both the gill and the digestive gland. This increase was correlated strongly with the levels of Cd accumulation measured in these tissues (R=0.957 for gill, 0.964 for digestive gland). Catalase activity followed a similar pattern, although the correlation with tissue Cd accumulation was not as strong (R=0.907 for gill, 0.708 for digestive gland) as that for MTLP. Lipid peroxidation increased in the digestive gland at Days 7 and 14 at both subchronic Cd levels tested, but this effect had largely dissipated by Days 21 and 28 (with the exception of the 2000μgL−1 group at Day 28). Alkaline phosphatase activity decreased significantly with Cd exposure in both tissues. This effect was observed at both tested concentrations in the gill, but only at the highest concentration for digestive gland. A decrease in digestive gland glycogen levels was observed in Cd-exposed mussels (Days 14 and 21 at 2000μgL−1), while haemolymph protein levels increased as a result of subchronic Cd exposure. These findings indicated that biochemical responses in Cd-exposed mussels were tissue-specific, dose- and time-dependent, with duration of e