Methamphetamine causes acute toxicity in the retina of Balb/c mice.

As a powerful psychostimulant with high potential for abuse, methamphetamine (Meth) could cause neurological diseases. METH-induced ophthalmic complications are present, but its underlying mechanism has not been completely elucidated, specifically on the retina. This study was to investigate effects of Meth treatment on the retina. Balb/c mice were treated with Meth at progressively increasing doses (0-6 mg/kg) intraperitoneally four times per day for five days, mice treated with saline as negative control. Electroretinography (ERG) was used to test the function of retina after Meth treatment. Pathological changes were examined by haematoxylin and eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the norepinephrine and tumour necrosis factor alpha (TNFα). Real-time PCR and western blot were used to measure expression changes of genes and proteins, respectively. Our data showed that Meth treatment caused photoreceptor cell death and decreased the thickness of retina. Meth treatment also elevated norepinephrine levels in plasma and increased TNFα in the retina. Moreover, Meth treatment decreased platelet endothelial cell adhesion molecule-1 (PECAM-1) protein expression and increased protein expression of matrix metalloproteinases (MMPs) in the retina. Our study indicated that short-term intraperitoneal treatment of Meth induced retinal degeneration of Balb/c mice due to a vascular loss of PECAM-1 and an increase of MMPs.