Palladium uptake and its effect on behavioural and molecular markers in the freshwater shrimp Gammarus pulex

The expanded use of platinum group elements (PGEs), platinum (Pt), palladium (Pd), and rhodium (Rh), in automobile catalysts has led to increased levels of these metals in aquatic environments. However, data regarding acute toxicity and the sublethal effects of these metals on aquatic biota are limited. This study aimed to explore the response of the freshwater amphipod Gammarus pulex to PGEs. Investigations included the 96 LC50 test and several behavioural (vertical movement and feeding activity) and biochemical (acetylcholinesterase (AChE); osmoregulation; 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) reduction; reduced glutathione (GSH); glutathione-S-transferase (GST); thiobarbituric acid reactive substances (TBARS); heat shock proteins (HSPs) and protein phosphorylation) endpoints. Pd caused a significant reduction in the survival of G. pulex with a 96 h LC50 of 0.52 mg/L (4.89 μM). Pt or Rh increased the survival of G. pulex exposed to Pd. However, this was not associated with reduced Pd uptake. Exposure for 24 h to 0.5 mg/L Pd (4.69 μM) significantly decreased the vertical movement (64%) and feeding activity (95%) of G. pulex. However, lower Pd concentrations (≥0.25 mg/L (2.3 μM)) took 72 h to induce significant inhibition in feeding activity (50%). AChE activity was significantly increased (40%) following 72 h exposure to 0.5 mg/L Pd. GST activity was significantly inhibited (≥32%) following 72 h exposure to ≤0.25 mg/L Pd. The concentration of GSH was significantly increased (22 and 35%) following 72 h exposure 0.1 (0.94 μM) and 0.5 mg/L Pd2+, respectively. Exposure to ≤0.1 mg/L Pd caused a significant decrease (≤27%) in MTT reduction and significant increase (≤70%) in HSP60 content in mitochondrial extract (pellet) after 72 and 24 h exposure, respectively. The reactivity of anti-phosphoserine bodies with protein bands corresponding to 245 kDa in the pellet was significantly increased (38%) by exposure of gammarids to 0.5 mg/L Pd. Exposure to 0.1 mg/L Pd significantly increased (32%) the intensity of a 30 kDa anti-phosphothreonine reactive protein band in the post-mitochondrial extract, but higher Pd doses had no effect. In conclusion, this study provides original data suggesting the mitochondria as a main target of Pd toxicity. Further studies of Pd toxicity, under both laboratory and field conditions, are needed including the effect of long-term exposure to low Pd concentrations.

Name dc:type.qualificationname

phd

Level dc:type.qualificationlevel

doctoral

Grantor dc:publisher.institution

Nottingham Trent University

Year dc:date.issued

2015

Author dc:creator

• Mohamed, WFA

Language dc:language

en