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ARTICLES
Year : 1980  |  Volume : 28  |  Issue : 1  |  Page : 5-7

Enzymatic studies on the galactose exposed lens


Zoology Department School of Sciences Gujarat University, Ahmedabad, India

Correspondence Address:
U M Rawal
Zoology Department School of Sciences Gujarat University, Ahmedabad 380009
India
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Source of Support: None, Conflict of Interest: None


PMID: 7203599

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How to cite this article:
Rawal U M, Rao G N. Enzymatic studies on the galactose exposed lens. Indian J Ophthalmol 1980;28:5-7

How to cite this URL:
Rawal U M, Rao G N. Enzymatic studies on the galactose exposed lens. Indian J Ophthalmol [serial online] 1980 [cited 2020 Oct 21];28:5-7. Available from: https://www.ijo.in/text.asp?1980/28/1/5/31037

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Studies on experimental galactose cataract in rats revealed a decrease in the lenticular energy metabolism [1],[2],[3]. During the develop­ment of galactose cataract, Sippel[4] noticed change in water, protein and glutathione contents of the lens in vivo. In vitro studies the decrease was found in the contents of free amino acids, free myo-inositol, glutathione ascorbic acid, sulfhydryl groups (-SH) and RNA in the lenses exposed to galactose."" The knowledge on the metabolic alterations in the course of galactose cataract and the changes that accompany in the lenses exposed to galactose is, however, useful. Such studies will provide basic information for interpreting and supporting a hypothesis on the mechanism of cataract formation. Therefore, the present investigation was mainly undertaken to see the effect of galactose, a sugar cataractogenic substance, on the enzymatic activities of glucose-6-phosphate (E.C. 1.1.1.49) and succi­nate (E.C.1.3.99.1) dehydrogenases (SDH) in the lenses of two species of laboratory animals.


  Materials and methods Top


Full grown adult rats (Rattus norvegicus Berkenhaut) and guinea pigs (Cavia porcellus Linnaeus) maintained in the laboratory on standard feeds (Hindustan Lever Ltd) were used throughout the investigation. Preparation of medium for lens culture and removal of the lenses were similar as described earlier.[6],[7]

Two parallel sets of experiments were con­ducted. In one set, lenses were cultured in the media having 20 mM galactose. In another, the counter lenses of the same animals were cultured in the media without galactose. Aseptic conditions were maintained wherever necessary and all the experiments were carried out at 35 + 1°C. In both the sets, lenses were harvested at 4 hours intervals upto 24 hours and used for the determinations of glucose-6­phosphate and succinate dehydrogenases acti­vities using Ells and .Kirkman's[8] and Kun and Abood's[9] methods respectively.


  Results Top


[Table - 1] presents the results of G-6-PDH and SDH activities in the lenses of two species of laboratory animals, rat and guinea pig, treated with and without galactose (20 mM). The activity of G-6-PDH showed a significant fall in the samples harvested after a minimum hours (4 hours) of galactose treatment in both the rat and guinea pig lenses. In contrast to G-6-PDH, the activity of SDH was found decreased significantly in the samples harvested after 16 hours and onwards in the case of rat and 12 hours and above after galactose treat­ment in the case of guinea pig lenses. However, the samples harvested after 20 and 24 hours of galactose treatment showed a marked decrease in both the enzyme activities of rat and guinea pig lenses. On the other hand, the contral­ateral lenses treated as control, exhibited nearly constant values for both the enzyme activities [Table - 1].


  Discussion Top


This investigation shows an inhibitory effect of galactose on both the G-6-PDH and SDH enzyme activities of rat and guinea pig lenses. Since the metabolism of glucose-6­phosphate via hexosemonophosphate shunt pathway depends mainly on the activity of G-6-PDH, it is suggested that the inhibitory effect of galactose on the activity of G-6-PDH may disturb the hexosemonophosphate path­way. The decreased activities of SDH in the galactose treated lenses as compared to control lenses also reveals an adverse effect of galactose on the citric acid cycle. By this study it is also known that the activity of G-6-PDH is more susceptible to galactose than the SDH activity. In vivo studies[10],[3] suggested that as the concentration of galactose penetrating the lens from the aqueous humour increases, the rate of reduction of galactose increases and dulcitol accumulates. The continuous produ­tion of dulcitol which leaks out of the lens very slowly and which is not further metabo­lised leads to the existence of its high levels within the fibres and specialiy in epithelial cells.[10],[3] Further, the accumulation of dulcitol disturbs the osmotic pressure, which in turn leads to a change in metabolic activities. It is obvious that the decreased activities of G-6-PDH and SDH in the galactose exposed lenses disturb the metabolism in the lens. These decreased enzyme activities in the galactose treated lenses could be due to the competence of galactose to some substrates or suppressions of some enzyme activities with the activation of the enzymes involved in its own metabolism or by the retention of its end product dulcitol.


  Summary Top


The effect of galactose on the activities of glucose-6-phosphate and succinic acid dehy­drogenases in the lenses of rat and guinea pig has been studied. These two enzymes showed decrease in their activities in the galactose treated lenses as compared to their controls. The activity of glucose-6-phosphate dehydro­genase was more susceptible to galactose than the activity of succinic acid dehydrogenase.

 
  References Top

1.
Kinoshita, J,H., 1965, Invest. Ophthalmol. 4: 786.  Back to cited text no. 1
    
2.
Van Heyningen, R., 1969, In the Eye 2 ndsub edition (Davson, H. ed) 381-400, 431-444, Academic Press, New York.  Back to cited text no. 2
    
3.
Van Heyningen, R., 1971. Exp. Eye Res., 11: 415.  Back to cited text no. 3
    
4.
Sippel, T.O., 1966, Invest. Ophthalmol, 5: 568.  Back to cited text no. 4
    
5.
Kinoshita, J.H., Barber, G.W., Merola, L.O. and Tung, B., 1969, Invest Ophthalmol, 8, 625.  Back to cited text no. 5
    
6.
Rawal, U.M. and Rao, G.N. 1979, Ind. J Exp. Biol 17: 91.  Back to cited text no. 6
    
7.
Rawal, U.M. and Rao, G.N., 1978, Indian J. Exp. Biol. 16: 499.  Back to cited text no. 7
    
8.
Charlton, J.M. and Van Heyningen, R., 1971, Exp. Eye Res., 11: 147.  Back to cited text no. 8
    
9.
Friedburg, D., 1972. Ophthalmic. Res., 3: 224.  Back to cited text no. 9
    
10.
Van Heyningen, R. , 1959, Biochem. J., 73: 197.  Back to cited text no. 10
    



 
 
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