TY - JOUR
T1 - Effects of Acute and Subchronic Waterborne Thallium Exposure on Ionoregulatory Enzyme Activity and Oxidative Stress in Rainbow Trout (Oncorhynchus mykiss)
AU - Nagel, Andrew
AU - Cuss, Chad W.
AU - Goss, Greg G.
AU - Shotyk, William
AU - Glover, Chris N.
N1 - Publisher Copyright:
© 2023 SETAC.
PY - 2024/1
Y1 - 2024/1
N2 - The mechanisms of acute (96-hour) and subchronic (28-day) toxicity of the waterborne trace metal thallium (Tl) to rainbow trout (Oncorhynchus mykiss) were investigated. Specifically, effects on branchial and renal ionoregulatory enzymes (sodium/potassium adenosine triphosphatase [ATPase; NKA] and proton ATPase) and hepatic oxidative stress endpoints (protein carbonylation, glutathione content, and activities of catalase and glutathione peroxidase) were examined. Fish (19–55 g) were acutely exposed to 0 (control), 0.9 (regulatory limit), 2004 (half the acute median lethal concentration), or 4200 (acute median lethal concentration) µg Tl L–1 or subchronically exposed to 0, 0.9, or 141 (an elevated environmental concentration) µg Tl L–1. The only effect following acute exposure was a stimulation of renal H+-ATPase activity at the highest Tl exposure concentration. Similarly, the only significant effect of subchronic Tl exposure was an inhibition of branchial NKA activity at 141 µg Tl L–1, an effect that may reflect the interaction of Tl with potassium ion handling. Despite significant literature evidence for effects of Tl on oxidative stress, there were no effects of Tl on any such endpoint in rainbow trout, regardless of exposure duration or exposure concentration. Elevated basal levels of antioxidant defenses may explain this finding. These data suggest that ionoregulatory perturbance is a more likely mechanism of Tl toxicity than oxidative stress in rainbow trout but is an endpoint of relevance only at elevated environmental Tl concentrations. Environ Toxicol Chem 2024;43:87–96.
AB - The mechanisms of acute (96-hour) and subchronic (28-day) toxicity of the waterborne trace metal thallium (Tl) to rainbow trout (Oncorhynchus mykiss) were investigated. Specifically, effects on branchial and renal ionoregulatory enzymes (sodium/potassium adenosine triphosphatase [ATPase; NKA] and proton ATPase) and hepatic oxidative stress endpoints (protein carbonylation, glutathione content, and activities of catalase and glutathione peroxidase) were examined. Fish (19–55 g) were acutely exposed to 0 (control), 0.9 (regulatory limit), 2004 (half the acute median lethal concentration), or 4200 (acute median lethal concentration) µg Tl L–1 or subchronically exposed to 0, 0.9, or 141 (an elevated environmental concentration) µg Tl L–1. The only effect following acute exposure was a stimulation of renal H+-ATPase activity at the highest Tl exposure concentration. Similarly, the only significant effect of subchronic Tl exposure was an inhibition of branchial NKA activity at 141 µg Tl L–1, an effect that may reflect the interaction of Tl with potassium ion handling. Despite significant literature evidence for effects of Tl on oxidative stress, there were no effects of Tl on any such endpoint in rainbow trout, regardless of exposure duration or exposure concentration. Elevated basal levels of antioxidant defenses may explain this finding. These data suggest that ionoregulatory perturbance is a more likely mechanism of Tl toxicity than oxidative stress in rainbow trout but is an endpoint of relevance only at elevated environmental Tl concentrations. Environ Toxicol Chem 2024;43:87–96.
KW - Aquatic toxicology
KW - Metal toxicity
KW - Toxicity mechanisms
UR - http://www.scopus.com/inward/record.url?scp=85174504335&partnerID=8YFLogxK
U2 - 10.1002/etc.5756
DO - 10.1002/etc.5756
M3 - Journal Article
C2 - 37750573
AN - SCOPUS:85174504335
SN - 0730-7268
VL - 43
SP - 87
EP - 96
JO - Environmental Toxicology and Chemistry
JF - Environmental Toxicology and Chemistry
IS - 1
ER -