The effects of chronic and acute exposure to hydrogen sulphide on Atlantic salmon (Salmo salar L)

• Main Authors: Kiemer, M C B, Black, Kenny, Lussot, D, Bullock, A M, Ezzi, Ivan
• Format: Article in Journal/Newspaper
• Language: English
• Published: 1995
• Subjects: NEOPLASMS; DETOXIFICATION; TROUT SALVELINUS-FONTINALIS; Marine & Freshwater Biology; Fisheries; ACCLIMATION; PROGRESSION; TOXIC-CHEMICALS; TIME COURSE; FISH; PUGET SOUND; SULFIDE TOLERANCE; Atlantic salmon; Salmo salar
• Online Access: https://pure.uhi.ac.uk/en/publications/77b02df8-339c-4967-9af7-19f886abb9d3

In separate experiments, Atlantic salmon smelts (Salmo salar L.) were exposed to two different regimes of hydrogen sulphide. In the first experiment, fish were exposed to chronic, periodic but sublethal levels of hydrogen sulphide (maximally 7.8 mu M) over a period of 18 weeks. Regular gill and liver samples were taken and growth determined relative to a control group. The difference in growth rate between treated and control fish was small. Gill damage (clubbing, thickening of the secondary lamellae) peaked between 6 and 8 weeks after initial exposure. Subsequently there was evidence of an adaptive response such that after 16 weeks, gill tissues from exposed fish appeared healthy and normal. Liver damage was progressive, By Week 10 more than 50% of livers examined showed diffuse hepatic necrosis and diffuse vacuolar degeneration which increased to 80% by Week 18. In the second experiment, salmon were exposed to one, single, acute but sub-lethal dose (22 mu M or 29 mu M) of hydrogen sulphide over 20 min. The effect on gills, livers and lactate dehydrogenase (LDH) activity was monitored over 14 days. For both concentrations, three salmon were sampled immediately, 1, 2; 3, 4, 6, 8, 10, 12 and 14 days after treatment. Gill tissues showed fusion of the secondary lamellae and thickening of the primary lamellae. Liver damage became evident 3 days after exposure. LDH activity was elevated compared to control for 4 days after exposure.