I Ololade, O Oginni
96-hr lc50, acute toxicity, fish, nickel, stress
I Ololade, O Oginni. Toxic Stress of Nickel on African Catfish, Clarias gariepinus Fingerlings. The Internet Journal of Veterinary Medicine. 2008 Volume 6 Number 1.
Toxic stress in
The fact that nickel is a natural element in the earth's makeup must be a factor in assessing its ability to harm the environment. Substances synthesized and released by humans represent a far more serious challenge for ecological systems than do natural substances simply because synthetic substances are new additions to the environment and organisms may not have developed coping mechanisms for them. It is important to note that simply being natural does not necessarily protect the environment from high additional fluxes of such substances from human activities. The ability of organisms to withstand some increase and the threshold point where toxic effects occur are the subjects of ecotoxicology. Nickel can do no harm (or benefit) to an organism unless the organism absorbs the divalent nickel ion into its body or the nickel ion is bound strongly enough to a membrane (fish gills) so that the membrane cannot function properly. Though, aquatic ecotoxicity testing has shown that NiSO4.6H2O and NiCl2.6H2O fall into the “harmful” classification which when abnormally high in concentration, can become toxic and can disturb the homeostasis of an animal (Farkas et al
It follows logically from this recognition that the total concentration of nickel in an environmental setting (aquatic or terrestrial) is not correlated with nickel's biological effects. Only the bioavailable portion of the nickel is relevant for ecotoxicity. While a condition might be constructed in a laboratory where nickel in a given medium is 100% bioavailable, it is virtually impossible to have such a situation under any naturally occurring conditions. In the natural environment there exists a complex group of reactants which are able to bind nickel into complex ions, precipitate nickel into insoluble compounds, adsorb nickel strongly to their surfaces, all of which remove the bioavailable nickel divalent ion from the medium by converting the nickel into another form which is not bioavailable.
The aquatic environment where fish and other aquatic organisms live is subjected to different types of pollutants which enter water bodies through industrial, domestic and agricultural discharge systems thereby introducing stress to living creatures. Stress is a general and non-specific response to any factor disturbing homeostasis. Stress reaction involves various physiological changes including alteration in blood composition and immune mechanisms (Svoboda 2001). It has also been linked as one major factor of disease outbreaks, low productivity and mortality in aquaculture (Rottman et al., 1992). Other toxic endpoints include decreased growth, mobility and reproductive effects (Allen, 1995). Stress in fish may be induced by various abiotic environmental factors (changes in water temperature, pH, O2 concentration and pollution). Changes in environmental quality can therefore be a major determinant of year-class strength and eventually the long-term dynamics of many fish populations (Rose
Fish have been the most popular choice as test organisms because they are presumably the best-understood organisms in the aquatic environment (Buikema
This work is therefore aimed at assessing the toxic stress of nickel on fish using a static bioassay technique (Reish and Oshida, 1987). The fish
Materials And Methods
Materials and Methods
Healthy specimens of African catfish
Water was changed every other day. The mean temperature, pH, alkalinity, hardness and dissolved oxygen of the water used were 27.40C, 6.51, 193.3 mg/L (as HCO3 -), 227.5mg/L as CaCO3 and 6.56 mgO2/L respectively. Ten fingerlings were kept per bowl. There were five different treatment groups and each had three replicates. The fish were fed three times daily. Feeding was discontinued while aeration continued during the 96-hr test period.
Stock solution of the test metal compound, a chemically pure nickel tetraoxosulphate IV hexahydrate (NiSO4.6H2O) was prepared by dissolving 4.5g of Merck grade reagent equivalent to 1 g of nickel in 1000 ml distilled water at concentration of 1000 mg/L. From the stock solutions, different concentrations required were prepared after a range – finding test using a screening procedure. The 96-hr LC50 was found to be 8.87mg/L in
Five sets of ten fish each were subjected to serial dilutions of the stock solution of Ni (from 4mg/L – 12mg/L) in triplicates. Two sets of control (each consisting 10 fishes) which contains no toxicants were also set up. The test was performed by the semistic (renewal) bioassay method in which the exposure medium was exchanged every 24-hr to maintain toxicant strength and level of dissolved oxygen as well as minimizing the ammonia excretion levels during this experiment. Initially, the fish were observed at 1-hr intervals for the first 6-hr after which they were observed at 2-hr intervals. Dead fish were identified by an absolute lack of movement. They were removed as soon as this was noticed. No mortality was observed among control fish. The toxicity of the test chemical was determined using the logarithmic method of analysis (Litchfield and Wilcoxon, 1949).
Results And Discussion
The results of the physico-chemical parameters (mean values) measured are given in Table 1. Table 2 represents detail of mortality as recorded during the study. The estimation of the lethal concentration values (LC50) was carried out using the Logarithmic method (Litchfield and Wilcoxon, 1949). The 96-hr LC50 values were determined from the graph (Fig.1) to be 8.87mg/L. Fig.1 depicts the percentage mortality for different exposure periods at different concentrations of nickel sulphate (4.0 ppm - 12.0 ppm). The LC50 value of NiSO4.6H2O for the fish
A regular trend was generally observed in the mortality rate which increases with increased concentration. At the early stage (i.e. the first 24hr) of the toxicants introduction, all the fishes survive initial attack. This may be due to their protective adaptations and the hardy nature of
Nickel toxicity to aquatic life depends on the species, pH, water hardness and other environmental factors (Blaylock and Frank, 1979). The water pH and hardness which increases with increased concentration of toxicants showed significant direct relationships with 96-hr LC50 concentration of the fish. Skin damage i.e. body lesions associated with red spot disease as noticed especially after 72-hr with fishes within 8.0 – 12.0ppm is indicative of pH stress. It shows further that fish like
Efforts were made to carefully observe the behaviour of the fishes during the 96-hr study. Behavioural functions are generally quite vulnerable to contaminant exposures, and fish often exhibited these responses first when exposed to pollutants (Little
Several factors have been attributed to behavioral changes/abnormalities in fish exposed to heavy metals like Ni (U.S. EPA,1986). These include nervous impairment due to blockage of nervous transmission between the nervous system and various effector sites, paralysis and depression of respiratory centre due to enzyme dysfunction, and alteration of energy pathway which results in energy depletion (Singh and Reddy,1990).
Bioaccumulation is not a valid criterion for judging the ecotoxicity of nickel substances because nickel is an essential element for many organisms and these organisms would suffer if they did not have the ability to accumulate and utilize nickel. Additionally, as a naturally occurring element, many organisms have mechanisms for detoxifying Ni through sequestration, thereby accumulating Ni in a non-toxic form. However, while the fish physiologically adapted to this environmental stressor, this trend does not always reflect a state of normality. The mortality recorded in the study is considered a consequence of stress induced on the immune system of fish. Thus, slow toxic progress and long continuance can result into chronic toxic response.
The presented results indicate that a short-term exposure to high levels of nickel induced stress reaction in fish. The gradual changes at lower concentration of toxicants in fish behaviour reflected a transient stress induced osmotic imbalance. However, deep changes observed showed that stress reduced the immune potential of fish. This reduced immunological status which persisted resulted in higher mortality especially at higher concentrations. Thus, it seems that even an incidental toxic stress may result in a considerable increase in susceptibility of fish to infections. Hence, good knowledge of fish response to various stressors will be of greater help in improving production of fish and in providing information on ways of effectively controlling and monitoring stress in aquaculture.