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Excretion: Presence of ammonia and urea


ABSTRACT

The experimental procedure was done to determine the presence of ammonia and urea in the excreta of terrestrial animals whereby locust and rat excreta was used. Presence of urea was tested by boiling the sample and adding two drops of glacial acetic acid and 10 drops of 10% xanthydrol reagent to a little of the excreta solution. Presence of ammonia was tested by boiling excreta and adding Nessler’s reagent to a little of the excreta solution. Colours produced were compared to those of the pure solutions of urea and ammonia, with the locust having a low concentration of both ammonia and urea whilst the rat had a low concentration of urea but a high concentration of ammonia. The results may have been attributed to the environments the organisms are adapted to which determine the type of nitrogenous wastes an organism excretes.

Keywords: ammonia, urea, uric acid, excretion, terrestrial organisms.

INTRODUCTION

The four major macromolecules ingested by animals are catabolised by the body to give rise to end-products of oxidation, which include carbon dioxide, water (carbohydrates and fats) as well as nitrogen wastes (proteins and nucleic acids) (Schmidt-Nielsen, 1990). Animals excrete a lot of nitrogenous wastes, predominantly, ammonia, urea and uric acid (Wright, 1995). The nitrogenous waste excreted by the animal depends on the habitat of the animal, that is, terrestrial, marine or freshwater. Generally, aquatic animals excrete ammonia (ammonotelic) (Wright, 1995), due to its high solubility in water and ease of diffusion in cell membranes (Schmidt- Nielsen, 1990) whilst terrestrial animals have evolved mechanisms that allow them to detoxify the ammonia and convert it to non-toxic urea and uric acid (ureotelic and uricotelic respectively) (Schmidt-Nielsen, 1990).

Generally, tolerance of ammonia is high in aquatic animals in comparison to the terrestrial animals although high levels in their system may result in flaccid paralysis as noted in arctic char as levels were beginning to approach 2mmoll-1 (Lumsden et al., 1993). The ammonia varying between 0.05 and 1 mmoll-1 is relatively safe as noted in teleost fish (Wright et al., 1993). In most mammals, the opposite is true with levels greater than 0.05mmoll-1 having dire consequences which include: the interference with amino acid transport (Mans et al., 1983); disruption of cerebral blood flow (Andersson et al., 1981); impedance of excitatory amino acid neurotransmitter metabolism (Hindfelt et al., 1977); morphological shifts in astrocytes and neurones (Gregorios et al., 1985) as well as the substitution of the K+ ion in the ion exchange mechanisms in the body leading to the interruption of nerve conduction (Binstock & Lecar, 1969).

All those effects combined lead to convulsions, coma as well as death (Wright, 1995) which makes it imperative for animals to adopt mechanisms that make it easy to excrete ammonia at all costs. The aim of this experiment was to test the presence of urea and ammonia on the faeces of rats and locusts which are both terrestrial animals.

METHODS AND MATERIALS

As per practical schedule.

RESULTS

Urea test

The initial pure solutions of different concentrations of urea showed a difference in colours produced, with the 0.01% urea concentration test producing an off-white precipitate; 0.1% urea concentration test producing a white precipitate and the 1.0% urea concentration producing a white precipitate (Table 1).

Table 1: The results obtained after making pure solution of urea at different concentrations

Urea Concentration Colour Produced

0.01% Off-white precipitate

0.1% White precipitate

1.0% White precipitate

After performing the urea test on the faeces of the locust the colour correlated to that of the 0.01% of urea which was an off-white precipitate compared to that of the higher concentration of 0.1% and 1.0% which were a white precipitate.

The rat faeces also showed low concentration of the urea, colour obtained correlating to that of the 0.01% of urea.

Ammonia Test

The pure solution of ammonia was a brown precipitate after Nessler’s test.

The locust faeces gave a green precipitate in colour after testing for ammonia which did not correlate with the colour obtained after adding ammonium hydroxide to Nessler’s reagent which showed no ammonia was present.

The rat faeces obtained a brown precipitate in colour after testing for the presence of ammonia which showed a correlation with the colour obtained after adding ammonium hydroxide to Nessler’s reagent indicating the presence of ammonia.

DISCUSSION

Locusts are terrestrial organisms and these have evolved methods of converting ammonia to non- toxic nitrogenous excretory products which may be urea or uric acid. Low concentrations of ammonia may be attributed to this fact. The low concentrations of urea may have been due to the locusts producing uric acid, which was not tested for in the laboratory. Generally insects have adopted mechanisms to convert ammonia to uric acid which has contributed to their success in a bid to conserve water. Uric acid is slightly soluble in water thus water loss is low (Schmidt-Nielsen, 1990).

The production of urea or uric acid is also dependent on the diet of the organism. If an organism was not feeding a lot, the excreta would not contain a lot of the nitrogenous excretory products thus the release of the nitrogen from the body is low. In a bid to maintain the hemolymph pH in insects (Harrison & Kennedy, 1994), the urea concentration excreted was low which would explain the results obtained after testing the locusts’ excreta for the presence of urea.

Rats are also terrestrial animals and the expected result would be to have a low concentration of ammonia as much as possible in the excreta of the rat due to its toxicity, although this was not the case. This may be attributed to the rat adopting mechanisms to save energy (Brooker et al., 2008) rather than undergoing the ornithine cycle that allows the production of the urea. The metabolic rate of small mammals is relatively high thus the need to conserve energy. Organisms generally adopt certain mechanisms that allow them to survive in their existing environment thus the variety in the nitrogenous excretory products excreted by animals.

REFERENCES

Andersson, K, E., Brandt, L., Hindfelt, B., & Ljunggren, B. (1981). Cerebrovascular effects of ammonia in vitro. Acta physiol. Scand, 113, 349-353.

Binstock, L., & Lecar, H. (1969). Ammonium ion currents in the squid giant axon. Journal of general Physiology, 53, 342-361.

Brooker, R. J., Widmaier, E. P., Graham, L. E., & Stiling, P. D. (2008). Biology. New York: McGraw Hill Company.

Gregoris, J. B., Mozes, L. W., & Norenberg, M. D. (1985). Morphologic effects of ammonia in primary astrocyte cultures .II. Electron microscopic studies. The Journal of Neuropathology and experimental Neurology, 44, 404-414.

Harrison, J., & Kennedy, M. (1994). In vivo studies of the Acid-Base Physiology of Grasshoppers: The Effect of feeding state on Acid-Base and Nitrogen Excretion. Physiological Zoology, 67(1), 120-141.

Hindfelt, B., Plum, F., & Duffy, T. E. (1977). Effects of acute ammonia intoxification on cerebral metabolism in rates with portacaval shunts, J. chin. Invest, 59, 386-396.

Lumsden, J. S., Wright, P. A., Derken, J., Byrne, P, J., & Ferguson, H. W. (1993). Paralysis in formed Arctic char (Salvelinous alpinus) associated with ammonia toxicity. Vet Record, 133, 422-423.

Mans, A. M., Biebuyk, J. F., & Hawkins, R. A. (1983). Ammonia selectively stimulates neutral amino acid transport across blood-barrier. Am J Physiol, 245, C74-C77.

Schmidt-Nielsen, K. (1990). Animal Physiology. Cambridge: Cambridge Press.

Wright, P, A. (1995). Nitrogen Excretion: Three end-products, many physiological roles. The Journal of Experimental Biology, 198, 273- 281.

Wright, P. A., Iwama, G, K., & Wood, C. M. (1993). Ammonia and urea excretion in Lahontan cutthroat trout (Incorhynchus clarki henshawi) adapted to the highly alkaline Pyramide Lake (pH 9.4). The Journal of Experimental Biology, 175, 153-172.

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