Sublethal Cobalt Toxicity Effects on Rainbow Trout (Oncorhynchus mykiss)

Abstract

The purpose of this study was to investigate the sublethal Co toxicity on rainbow trout (Oncorhynchus mykiss). Trout were exposed to Co and selected parameters were evaluated at intervals of 1, 15 and 30 days. Fish exposed to higher levels of Co grew slower than fish exposed to lower levels of Co. Weight gain, specific growth rate (SGR) decreased linearly with the increase of cobalt in the water. The body condition factor (CF) of fish reared in water with low cobalt concentration decreased substantially but this decrease was not significant for fish exposed to higher cobalt concentration. The values of the feed conversion ratio (FCR) increased in fish exposed to higher levels of Co. Co significantly changed the activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and decreased at day 30, and in both cases this decrease was more remarkable at day 15 so that the level of AST and ALT reached the control value at day 30. The alkaline phosphatase (ALP) level also showed a remarkable 15-day decline. There was a significant increase in glucose (G) concentration in both Co-exposed groups on day 15. However, serum cholesterol (Chl) was significantly reduced on day 15 and increased on day 30; there were no significant differences in both exposed Co-groups. The triglyceride (TG) level also decreased substantially. There was no regular pattern of total protein (TP) in the serum, so that no significant differences were found in the level of TP between low and high-exposed fish. In summary, this study suggests that exposure of essential trace elements such as cobalt may change growth and biochemical parameters, and that measurement of these parameters may be used in toxicological studies to determine the general health status of fish.

Comprehensive Assessment and Potential Ecological Risk of Trace Element Pollution (As, Ni, Co and Cr) in Aquatic Environmental Samples from an Industrialized Area

“…Co is a cofactor for many enzymes and its toxicity to fish appears to be relatively low compared to the effects of other metal ions, particularly during short-term exposures. Cobalt toxicity causes heme oxidation and inhibition of inorganic calcium channels in fish gills [ 69 ]. Arsenic can accumulate in different tissues in various organic forms, with a low percentage in the more toxic inorganic form.…”

Differential effects of cobalt ionsin vitroon gill (Na+, K+)-ATPase kinetics in the blue crabCallinectes danae(Decapoda, Brachyura)

“…Cobalt titers in brachyuran crabs from marine/estuarine ecosystems range from 0.26 to 0.43 µg Co 2+ g -1 soft tissue dry mass in Callinectes sapidus [32]; 0.91 to 1.2 µg Co 2+ g -1 hepatopancreas dry mass in male and female Portunus segnis [33]; and 0.72 to 0.86 µg Co 2+ g -1 dry mass in whole Carcinus maenas [34]. The lack of molecular information regarding harm to aquatic organisms, including the effects of Co 2+ , has impaired our overall comprehension of environmental damage and particularly of toxicity owing to bioaccumulation in marine organisms [16,23,25,35].…”

“…While cobalt is a trace element indispensable for various physiological processes [21,23,24] it is toxic at high intracellular concentrations [25]. In humans, excessive exposure to cobalt results in complex health deficits involving heme oxidation, cytotoxicity, oxidative stress, apoptosis, altered membrane permeability, calcium channel blockage and DNA damage [26][27][28].…”

Caracterização cinética e molecular da (Na>sup<+>/sup<, K>sup<+>/sup<)-ATPase do tecido branquial de >i<Callinectes danae>/i< submetido a estresse por cobalto

“…O cobalto está presente nas fuções vitais como componente da molécula de vitamina B12 (Figura 9) (cobalamina), fundamental em diversos processos biológicos, principalmente na transferência de grupos metil para o DNA (Caçador et al, 2012;Nasri, Heydarnejad, Nematollahi, 2019;Zoroddua et al, 2019). Entre os problemas relacionados a deficiência de vitamina B12 estão a anemia perniciosa, patologias neurológicas e hematológicas (Yamada, 2013;Zoroddua et al, 2019), isso ocorre devido a inativação das enzimas metionina sintase e metilmalonil-CoA mutase, que são dependentes desta vitamina (Zoroddua et al, 2019).…”

“…Os íons de cobalto atuam bloqueando o transporte ativo de Ca 2+ nas brânquias em peixes de água doce e interferem nas vias metabólicas de algas de água doce (Niyogi, Wood, 2003). As escassas informações sobre os riscos potenciais do Co 2+ para o ambiente aquático, e informações insuficientes sobre o mecanismo de toxicidade tem prejudicado o conhecimento dos possíveis riscos ambientais que este íon pode causar, especialmente em organismos marinhos (Richards, 1988;Nasri, Heydarnejad, Nematollahi, 2019).…”