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| ORIGINAL ARTICLE |
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| Year : 1984 | Volume
: 32
| Issue : 1 | Page : 13-15 |
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Relationship of glucose-6-phosphate dehydrogenase with structural development and growth of human foetal cornea
Abhijit Sen, KL Mukherjee
Department of Biochemistry, lnstitute of Post Graduate Medical Education and Research, 244, Acharya J C. Bose Road Calcutta, India
Correspondence Address:
Abhijit Sen
Department of Biochemistry, Institute of Post Graduate Medical Education & Research, 244, Acharya J.C. Bose Road, Calcutta 700 020
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 6500658 
How to cite this article:
Sen A, Mukherjee K L. Relationship of glucose-6-phosphate dehydrogenase with structural development and growth of human foetal cornea. Indian J Ophthalmol 1984;32:13-5 |
Cornea is both ecto and mesodermal in origin. The enzyme glucose-6 phosphate dehydrogenase belongs to the hexose monophosphate shunt which is essential for the synthesis of ribose, deoxyribose and reduced NADP, required for lipid synthesis. The G-6-PD activity is absent in stromal keratocyte.[1]1 The hexose" monophosphate shunt activity is primarily located at the epithelial layer of cornea.[2] About 70% of glucose oxidation in the corneal epithelium accounts for hexose monophosphate shunt[3] The D-ribose-5-phosphate generated by the pathway is used in the nucleic acid synthesis and the reduced NADP is used for the synthesis of -the lipid content of cell membrane of the corneal epithelium. An attempt is made to analyse and co-relate the histological development with glucose-6phosphate dehydrogenase level of human foetal cornea.
| Materials and methods | |  |
The human fetuses were obtained from the M/T/P Clinic of the Department of Obstetrics and Gynaecology. They were taken out of the uterus in their entirety by hysterotomy in, multiparous mother who did not want to' continue their pregnancy and also opted for ligation at the same time. Informal consents were obtained from the mothers for the use of their fetuses and the project was cleared by the ethical subcommittee of the Institute. Normal fetuses obtained from mothers in good health were selected for the present study.
The eyes were immediately enucleated, the entire cornea of one eye was dissected out, weighed to the nearest tenth of a milligram and used for the biochemical estimation. The other eye was used for the study of histological development of cornea. The G-6-PD activity of cornea was estimated by the method of Warburg et al.[4] The histology of cornea was studied by staining with eosin and haematoxylin.
| Observations | | |
Histological development of human fetal cornea was followed from 7 to 24 weeks of gestation by haemotoxylin-eosin staining. The surface ectoderm which remains near the optic cup, forms the corneal epithelium. The lens vesicle which appears in the inner side of surface ectoderm gets detached from it and forms the lens. Mesodermal invasion starts below the developing cornea
The differentiation of these cells transform it into a fully formed cornea.
[Table - 1] shows the anthropometry of the fetuses and their G-6-PD content. The G-6PD content was found to increase gradually from 0.45 µM/minute/gm. protein of cornea at 9 weeks to 2.5 µM/minute/gm. protein of cornea at 16 weeks of gestation which stayed at this level up to 24 weeks of gestation. Estimation of G-6-PD level of fetuses above 24 weeks of gestation could not be undertaken on account of lack of availability of suitable fetuses at that age group. Likewise study with gestational period of less than 7 weeks were left out due to technical difficulty in the dissection of cornea at this period. The specific activities of G-6-PD of foetal ophthalmic tissue is lower than that of foetal liver.
The G-6-PD level of adult cornea is almost double the level of fetal cornea and more than that of adult liver. The relationship of fetal body weight with the G-6-PD activities of fetal cornea is shown graphically.
| Discussion | | |
Histological development of the cornea is characterized by an organised growth of surface epithelium, below which the mesodermal cells invaginate and become transformed into various layers of the cornea. The number of cells per unit area varies at different period of gestation. Presumably growth rate also varies paripassu. For growth, the syntheses of ribose and deoxyribose are necessary and the operation of G-6-PD shunt pathway would be needed.
The G-6-PD activity of cornea increase from a low level in earlier period to a high level around mid-gestation. This rapidly increasing level of G-6-PD is probably due to the greater demand made on it to meet the most active phase of growth of cornea at this period. In the later period of gestation the corneal growth rate is more or less steady as it . has already attained its histological maturity,' this keeps the G-6-PD level more or less the same. High G-6-PD level of adult cornea is probably due to its multi-layered epithelium which is the site of hexose monophosphate shunt for cornea.
Contrary to the observation of Masterson, et al[5], which was however on chick cornea, the human fetal corneas were observed to remain transparent during the period of gestation and no relationship could be established between the transparency of cornea and G-6PD level in human foetuses.
| Summary | | |
The histological development of healthy, human foetal cornea belonging to 9 to 24 weeks of gestation were studied in relation to G-6-PD level. G-6-PD activities of human fetal cornea gradually increased from 9 to 16 weeks and then stayed at that level up to 24 weeks of gestation. G-6-PD activities of human foetal cornea was lower than that of adult cornea. Human foetal corneas have been observed to remain transparent during the period of gestation.
| Acknowledgement | | |
Grateful acknowledgement are due to Prof. S.K. Bhattacharjee, Head of the Department of Obstetrics and Gynaecology for making the fetuses available to us and to Mr. Santanu Sen of I.E.G. Consultants (Pvt. Ltd.) for kind assistance in analysing the' statistical data. The study was supported by the I.C.M.R, New Delhi.
| References | | |
| 1. | Baum, J.L. 1963, Arch. Ophthalmol 70: 59.  |
| 2. | Kinoshita, J.H. 1962, invest. Ophthalmol 1: 178. |
| 3. | Kuhlman, RE. and Resnik, RA. 1959, Arch.Biochem. Biophys. 85: 29. |
| 4. | Warburg, O., Christian. W., and Griese. A., 1935. Biochem. A. 282: 157. |
| 5. | Masterson. E., Edelhouse, H.F. and Chander. G.J., 1978, Biochim. Biophys. Acta. 542: 372. |
[Table - 1]
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