|Year : 1980 | Volume
| Issue : 1 | Page : 1-3
Effect of 'catalin' an anticataract agent on alloxan induced hyperglycaemia and diabetic cataract in rats
PM Bulakh1, AG Chandorkar2, JJ Balsara3, SM Ranade1, MV Albal3
1 Department of Biochemistry, Dr. V. M. Medical College, Solapur, India
2 Department of Ophthalmology, Dr. V. M. Medical College, Solapur, India
3 Department of Pharmacology, Dr. V. M. Medical College, Solapur, India
A G Chandorkar
Department of Pharmacology, Dr. V.M. Medical College, Solapur-413003
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Bulakh P M, Chandorkar A G, Balsara J J, Ranade S M, Albal M V. Effect of 'catalin' an anticataract agent on alloxan induced hyperglycaemia and diabetic cataract in rats. Indian J Ophthalmol 1980;28:1-3
|How to cite this URL:|
Bulakh P M, Chandorkar A G, Balsara J J, Ranade S M, Albal M V. Effect of 'catalin' an anticataract agent on alloxan induced hyperglycaemia and diabetic cataract in rats. Indian J Ophthalmol [serial online] 1980 [cited 2020 Oct 21];28:1-3. Available from: https://www.ijo.in/text.asp?1980/28/1/1/31036
Catalin (1. hydroxy-5-oxo-5.4 Pyrido phenoxazoline 3-Carboxylic acid) a recently introduced anticataract agent, has been shown to be effective in arresting the development of senile and diabetic cataracts,,,,,,,, Although this effect has been denied in senile cataract. In our preliminary study, we have reported on the hypoglycaemic effect of catalin. Hence, the present investigation was undertaken to evaluate its mechanism as hypoglycaemic agent as well as anticataract effects on alloxan induced hyperglycaemia and alloxan induces diabetic cataracts.
| Material and methods|| |
Twenty four rats of either sex weighing between 100-200 G were used for the study. The animals were injected with alloxan in dose of 50 mg/kg given intravenously through the tail vein and were divided into control and ,'rug treated groups. Catalin was administered to the drug treated animals daily, in a dose of 20 mg/kg, intraperitoneally (I.P.) daily for six weeks. White the control group received normal saline I.P. daily instead of the drug. Volume of the drug solution was adjusted in such a way that it never exceeded 0.5 ml. solution of alloxan was prepared fresh, just before the injection for each animals.
Animals were sacrificed at the end of 5th. & 6th. weeks and the blood sugar level was estimated by the colorimetric method of Folin & Wu. The eyes were examined every 3rd. day for development of opacities during the entire course of study. The lenses were removed after sacrificing the animals and the observations were confirmed in vitro.
Another group of twelve normal rats kept under identical conditions were also sacrificed and their blood sugar levels were estimated and their lenses extracted to study the normal physiological pattern. This was used as basis for comparison with the results obtained with alloxan treated animals.
| Results|| |
It was observed that the normal fasting blood sugar level ranged from 70-96 mg% with a mean of 82±0.4 SE. Pretreatment with alloxan in the control group induced a significant hyperglycaemia (with an increase of 65-72% in the base sugar level) in 91.6% of the animals. Daily administration of catalin 20 mg/kg I.P., however, reduced this incidence of hyperglycaemia to 51.6%. Alloxan pretreatment also induced the development of diabetic cataracts (hyperglycaemic) in 87.5% of the eyes as compared with the untreated animals. The opacities started developing mostly in both the eyes by the end of third week and progressed till the whole lens became opaque by the end of fifth week.
Administration of catalin in alloxan pretreated animals prevented the development of cataracts in 100% of the animals. However, some of the animals whose blood sugar was not adquately controlled by this dose of catalin, started developing small opacities by the end of fourth week [Figure - 2]. There was no significant change in the results at the end of the 6th. week as compared to that seen at the end of 5th. week.
| Discussion|| |
Alloxan is known to produce selective degeneration and degranulation of Beta-cells of Islet of Langerhans in pancreas and hence produces a hyperglycaemic state resembling diabetes and in this study induced hyperglycaemia in 91.6% animals.
The failure of alloxan to induce significant hyperglycaemia in 8.4% animals may be due to its failure to damage enough number of Beta-cells after I.P. injection, as its half life is hardly few seconds and hence some of the Beta-cells might have escaped damage though fresh solution was prepared and injected each time.
Administration of catalin prevented development of hyperglycaemia in about 40% of the alloxan treated animals, hence it seems to act peripherally by producing an hypoglycaemic effect, probably similar in nature to that produced by biguanides, and definetely not through the Beta-cell stimulation and release of insulin as is seen with sulphonyl-ureacompounds.
Catalin was able to prevent the onset of development of diabetic cataracts in 100% of the eyes. This may also be due to its peripheral hypoglycaemic effects, as the development of diabetic cataracts depend on consistant high levels of blood glucose, which may then be reflected in increased intraocular or lenticular glucose levels. Failure of catalin in preventing development of cataracts in 18.4% eyes seen at the end of 5th. and 6th. weeks, is also in consistance with the above, as it seems Catalin could not sufficiently reduce the hyperglycaemic levels in these animals, below the threshold level of blood sugar required for development of cataracts in alloxan treated animals.
| Summary|| |
Catalin, a pyridophenoxazoline derivative, introduced as an anticataract agent was investigated for mechanism of hypoglycaemia and anticataract effect, on alloxan induced hyperglycaemia and alloxan induced diabetic cataracts in rats. Alloxan induced significant hyperglyeaemia in 91.6% of the animals at the end of 5th. week and also showed development of diabetic cataracts in 87.5% of the eyes.
Administration of catalin 20 mg/kg 1.P. prevented the onset of alloxan induced cataracts in l00% of the diabetic animals and reduced the incidence of hyperglycaemia to 51.6%. Effect of catalin seems to be due to its hypoglycaemic effect, which is periperal in nature probably similar to that of biguanides, as it is produced in alloxan treated animals and not through the stimulation of insulin release.
| Acknowledgement|| |
The authors are grateful to the Dean, Dr. V.M. Medical College, Solapur, for the facilities given to undertake this works and to M/s. SENJU Pharmaceutical Company, Japan, for the supply of catalin.
| References|| |
Albal, M.V., Chandorkar, A.G., and Jain P.K., 1976, ACTA 6th Afro-Asian Congress of Ophthalmology, p. 195.
Angra, S.K. (1976) ACTA 6th Afro-Asian Congress of Ophthalmology p. 200.
Asayama, R. Shirakami, T. and Amatsu, M., 1960 Jap. J. Clin. Ophthalmol., 14, 789.
Chandorkar A.G., Albal, M.V. Bulakh P.M., and Jain P.K., 1978, Ind. J. Ophthalmol., 26 (1), 6.
Komi. T. and Uchida, S., 1962, Jap. J. Clin. Ophthalmol., 14, 959.
Nishimura F. 1960, Jap. Rev. Clin. Ophthalmol., 54, 3, 255.
Nishimura, K. and Shimisu, H., 1958, Jap. Rev Clini. Ophthal., 52, 6, 576.
Ochial, T., 1966, Jap. Rev. Clin. Ophthalmol., 60, 7, 641.
Ogino. S., 1958, Jap. J. Clin. Ophthalmol., 12, 591.
[Figure - 1], [Figure - 2]