Electroretinogram and histopathologic changes of the retina after methanol intoxication.
- Author:
Jie-Min CHEN
1
;
Guang-You ZHU
;
Zi-Qin ZHAO
;
Wen-Tao XIA
Author Information
1. Shanghai Key Laboratory of Forensic Medicine, Institute of Forensic Science, Ministry of Justice, P.R. China.
- Publication Type:Journal Article
- MeSH:
Animals;
Edema/pathology*;
Electroretinography;
Forensic Medicine;
Male;
Methanol/poisoning*;
Mitochondria/pathology*;
Photoreceptor Cells/pathology*;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Retina/physiopathology*;
Retinal Cone Photoreceptor Cells/pathology*;
Retinal Diseases/pathology*;
Retinal Rod Photoreceptor Cells/pathology*;
Time Factors
- From:
Journal of Forensic Medicine
2013;29(1):5-16
- CountryChina
- Language:English
-
Abstract:
In order to study the functional and structural alterations of the retina in SD rat model after methanol intoxication, 35 rats were divided randomly into five groups administrated with saline, 3-day high dose, 7-day high dose, 3-day low dose and 7-day low dose methanol separately. The retinal function of each group was assessed by flash electroretinogram (F-ERG) 3 and 7 days after methanol poisoning. The microstructure and ultrastructure of the retina were observed at the same time. The high-dose methanol intoxication induced irreversible retinal functional and structural damages 3 days after poisoning, which included prolonged latency and reduced amplitude of the Max-reaction of F-ERG. These injuries were aggravated 7 days after poisoning. Meanwhile, the latency and amplitude of the Cone-reaction of F-ERG were also affected 3 days after poisoning, but there were no further worsening tendency 7 days after poisoning. The retinal histological analysis showed cellular edema, heteromorphy and disarrangement, tissular loosen of the inner nuclear layer and photoreceptors layer. The mitochondrial damage began at the photoreceptors layer and developed further into the inner nuclear layer. The low-dose methanol intoxication only caused transient damage of the retina. Our results showed that the function and structure of the photoreceptor and inner nuclear layer were the primary target of methanol intoxication and that the rod cells were more sensitive to methanol intoxication than the cone cells. The mitochondrial damage developed from outer layer to inner layer of the retina.
