Discussion on Copper Toxicity Effects in Pangasius Fry Respiration
Table of Contents
Introduction
Copper, an essential trace metal, becomes a potent toxicant when introduced into aquatic ecosystems at elevated concentrations. For freshwater species like Pangasianodon hypophthalmus — a commercially important edible fish — understanding how copper affects physiological functions such as respiration is critical for aquaculture sustainability and environmental health.
This blog post presents a detailed scientific discussion taken directly from a zoology thesis on the impact of copper toxicity on the oxygen consumption and metabolic rate in Pangasius fry.
The selected passage is rich in literature references, includes direct observations from the study, and draws connections to earlier toxicological findings.
It will be particularly useful for researchers in aquatic toxicology, environmental science students, and aquaculturists concerned with the sublethal effects of heavy metals.
The focus keyword “copper toxicity” is central to this analysis, recurring throughout the excerpt.
Excerpt (Unchanged Thesis Content
DISCUSSION
The results clearly depict inhibition in the routine oxygen consumption and routine metabolic rate in fish fry on exposure to sublethal levels of copper. Several investigators reported similar inhibition in the respiratory rate of different aquatic organisms including fishes and crustaceans on exposure to toxicants.
De Boeck et al. [2007] noticed that copper causes both respiratory and ion regulatory distress in spiny dog fish Squlus acanthius. Shwetha and Hosetti [2009] studied the acute effects of zinc on the behaviour and oxygen consumption of the Indian major carp Cirrhinus mrigala and reported that normal respiratory activity of the fish was significantly affected and there was a depression in the metabolic rates at the end of exposure periods [24, 48, 72 and 96 hrs].
Prashanth et al. [2010] investigated the impact of copper cyanide on behavioural changes and oxygen consumption in Catla catla and found that with increased concentration and time; the mortality rates have been increased accompanied by decreased oxygen consumption. Tilak and Satyavardhan [2002] observed the decrease in oxygen consumption at sublethal concentrations of copper in Channa punctatus indicating lowered energy requirements which in turn indicate pronounced biochemical changes.
Skidmore [1970] using cannulation technique found that zinc reduced the efficiency of oxygen transport across the gill membrane, so that fishes die of hypoxia. Deepak et al. (2011) while studying cadmium toxicity to fresh water cat fish, Heteropneustes fossilis, observed respiratory distress in fishes associated with opercular beats.
Metelev et al. (1983) reported that fish exhibits intense excitation and difficulty to respire in toxic solutions of copper. Lauren and Mc Donald (1985) studied effects of copper on branchial ion regulation in the rainbow trout, Salmo gairdneri (Rich) modulation by water hardness and pH. They noticed that high concentrations of water borne copper affect branchial function and the main toxic action being impairment of sodium homeostasis.
Hassan (2011) while studying the effects of sublethal concentrations of copper and cadmium (0.1, 0.25, 0.4 ppm) on the survival rate, oxygen consumption and histopathological changes in the gills of juvenile Cyprinus carpio (L.), showed a decreased oxygen consumption with increasing concentration and there was a negative correlation between oxygen consumption and metal concentration.
According to him, copper was found to be more toxic compared to cadmium.
A time-dependent and concentration-dependent decrease in oxygen consumption was reported by Appa Rao et al. [2009] in Cirrhinus mrigala on exposure to sublethal concentration of Dimethoate.
A significant correlation between the toxicant uptake and fish oxygen consumption was reported by Yang et al (2000). Vutukuru (2005) investigated the acute effects of hexavalent chromium on survival,
oxygen consumption in Labeo rohita and found deleterious effects at various vital functional sites like metabolic rate, haematological indices and biochemical profiles.
Similar decrease in oxygen consumption was observed in Pangasius fish fry of the present experiment at all intervals from 24 hrs to 30 days of exposure. It might be due to interaction of copper with mitochondria of the cells resulting depletion of oxygen consumption as reported by Webb (1979).
Earlier investigation on sublethal copper exposure revealed a time-dependent accumulation of metal substantiating the interaction of copper.
Total oxygen consumption is one of the indicators of the general well-being of the fish.
It is useful to assess the physiological and biochemical state of organism, to evaluate the susceptibility or resistance potentiality and to correlate the behavior of the animal, which ultimately serves as predictors of functional disruptions of animals in population.
Therefore, oxygen consumption analysis can be used as a biodetectory system to evaluate the basic damage inflicted on the animal which could either decrease or increase the oxygen uptake.
The metabolic rate of Pangasianodon fish fry in the present experiment decreased from 10 days to 30 days both in the control and exposed but this decrease was more pronounced in exposed fry. In control,
the decrease in metabolic rate can be attributed to increase in size, whereas in exposed fish the decrease might be due to increased metal accumulation along with increase in size.
It is reported that the heavy metals are known to depress respiratory rate possibly by direct metabolic inhibition (Brown and Newell, 1972; Delhaye and Cornet, 1975; Engel and Flower, 1979; Uma Devi, 1996).
However, the clear mode of action of the persisting metal against the respiratory response at different intervals is not clearly understood.
Source Citation
Researcher: Pratima Kumari, S
Thesis Title: Copper toxicity on fry of fresh water edible fish pangasianodon hypophthalmus
Supervisor: Prabhakara Rao, Y
University: Andhra University
Year of Completion: 2012
Exit Page Number: 85
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