TY - JOUR
T1 - Biochemical biomarker responses of green-lipped mussel, Perna canaliculus, to acute and subchronic waterborne cadmium toxicity
AU - Chandurvelan, Rathishri
AU - Marsden, Islay D.
AU - Gaw, Sally
AU - Glover, Chris N.
N1 - Funding Information:
This study was funded by the Brian Mason Scientific & Technical Trust. Jackie Healy is thanked for technical assistance. Our special thanks to Robert Alumbaugh and members of the Department of Pharmacology and Toxicology, University of Otago for their help towards completion of this study. We are grateful to Jacqui Lee for help with, and to Mauricio Urbina for initial consultation regarding, the NKA assay. RC is supported by a University of Canterbury Doctoral Scholarship .
PY - 2013/9/15
Y1 - 2013/9/15
N2 - 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 exposure being the predominant effect. This study shows that biochemical changes in Cd-exposed green-lipped mussels can be linked to tissue metal accumulation and are consistent with previously reported physiological effects. It also suggests that green-lipped mussels are amenable to a multiple biomarker approach and may be of use as a bioindicator species for monitoring coastal metal pollution.
AB - 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 exposure being the predominant effect. This study shows that biochemical changes in Cd-exposed green-lipped mussels can be linked to tissue metal accumulation and are consistent with previously reported physiological effects. It also suggests that green-lipped mussels are amenable to a multiple biomarker approach and may be of use as a bioindicator species for monitoring coastal metal pollution.
KW - Cadmium
KW - Enzyme biomarkers
KW - Glycogen
KW - Metallothionein-like protein
KW - Oxidative stress
KW - Perna canaliculus
UR - http://www.scopus.com/inward/record.url?scp=84880579325&partnerID=8YFLogxK
U2 - 10.1016/j.aquatox.2013.06.015
DO - 10.1016/j.aquatox.2013.06.015
M3 - Journal Article
C2 - 23876876
AN - SCOPUS:84880579325
SN - 0166-445X
VL - 140-141
SP - 303
EP - 313
JO - Aquatic Toxicology
JF - Aquatic Toxicology
ER -