Assessing the Effects of Increasing Hydrogen Peroxide Dosage on Rainbow Trout Gills Utilizing a Digitized Scoring Methodology

Characterization of the toxicity of Cochlodinium polykrikoides isolates from Northeast US estuaries to finfish and shellfish

“…Such degradation of the gill lamellae would prohibit gill function (i.e. gas exchange) and is nearly identical to the histopathological characteristics of fish killed by raw bloom water (Gobler et al, 2008) and to the damage incurred to fish gills exposed to lethal levels of reactive oxygen species (Tort et al, 2002). Importantly, C. polykrikoides cells exposed to peroxidase and catalase at the highest levels used in the bioassay remained viable and grew at rates equal to those of unamended cultures, suggesting compromised algal cells were not responsible for the significant decrease in toxicity of cultures.…”

Harmful dinoflagellate blooms caused by Cochlodinium sp.: Global expansion and ecological strategies facilitating bloom formation

“…respiration, nitrogen excretion, ion balance) of gill lamellae Tang and Gobler, 2009b). Such rapid degradation of the gill lamellae is characteristic of an external insult to the gills such as exposure to a parasite (Roberts, 2001) and is similar to the characteristics of fish gills exposed to lethal levels of ROS (Tort et al, 2002). Shellfish exposed to Cochlodinium for several days have displayed hyperplasia, haemorrhaging, squamation, and apoptosis in both gill and digestive tissues , indicating that Cochlodinium toxins target a broad range of organisms and tissue types.…”

Histological evaluation of sodium percarbonate exposure on the gills of rainbow trout

“…Gaikowski et al (1999) reported that the NOEC for HP in rainbow trout in 60 min exposures administered on Days 1, 3 and 5 at 12°C was 188 mg l −1 in fry and 162 mg l −1 in fingerlings, which is within the range of NOEC values for juvenile rainbow trout reported by Rach et al (1997) at 12°C. Tort et al (2002) reported that the LC 50 of HP to 30 to 60 d old rainbow trout during a single 60 min exposure was approximately 180 mg l −1 at 14°C. HP oxidises more rapidly with increasing water temperature (Rach et al 1997) and with decreasing pH (Bishop et al 1968), and is therefore more toxic at higher temperatures and lower pH.…”

“…Fish exposed to 250 mg l −1 SPC also had significantly more gill oedema after the fourth treatment than other treatment groups and controls. Rainbow trout exposed to ≥100 mg l −1 HP for 1 h displayed epithelial lifting and gill necrosis (Tort et al 2002) which can impair basic gill function including oxygen transport in high exposures (500 mg l −1 ) (Powell & Perry 1997). Derksen et al (1999) attributed epithelial cell swelling in the gills of rainbow trout exposed to HP to the oxidant effect of HP overcoming innate antioxidant defences.…”

“…However, results from in vitro trials indicated that doses above 100 mg l −1 are required to effectively control all free-living stages of I. multifiliis (see Forwood et al 2014a). The impacts of HP on Atlantic salmon Salmo salar (Salmonidae) (see Johnson et al 1993, Kiemer & Black 1997 and rainbow trout Oncorhynchus mykiss (Salmonidae) (see Speare et al 1999, Tort et al 2002 have been investigated, and results indicated that structural damage was restricted to the gills (Roth et al 1993, Kiemer & Black 1997, Tort et al 2002. Alkalinity and pH could affect the efficacy and host toxicity of HP treatment (Tort et al 2002), although the tolerance of rainbow trout to HP slowly released from SPC with significantly increased alkalinity from carbonate is unknown.…”