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Long-Term Systemic Treatment With Methamphetamine Causes Retinal Damage in CD1 Mice
Haojiang Yang1, Liming Tao1, Lin Li2
1Department of Ophthalmology, The Second Hospital Affiliated to Anhui Medical University, Hefei, People's Republic of China.
International Journal of Toxicology
|October 31, 2018
Summary
Methamphetamine (Meth) abuse causes long-term retinal damage in mice. This study reveals Meth induces photoreceptor cell loss, apoptosis, inflammation, and oxidative stress, leading to neurotoxic effects on the retina.
Area of Science:
- Ophthalmology
- Neuroscience
- Toxicology
Background:
- Methamphetamine (Meth) is a psychostimulant with high abuse potential.
- Meth abuse can lead to persistent retinal abnormalities.
Purpose of the Study:
- To investigate the effects of low-dose Meth on retinal damage.
- To elucidate the underlying pathological mechanisms of Meth-induced retinal damage.
Main Methods:
- CD1 mice received daily intraperitoneal injections of Meth (0.5 or 1 mg/kg) or saline for 2 months.
- Evaluated retinal function using electroretinography (ERG).
- Assessed retinal morphology, cell loss, apoptosis, inflammation, oxidative stress, and gene/protein expression via Toluidine blue staining, TUNEL assay, ELISA, qPCR, and Western blot.
Main Results:
- Meth treatment resulted in rod photoreceptor cell loss and decreased ERG amplitude.
- Increased photoreceptor apoptosis, cytochrome-c release, caspase-3 and -9 activity, and apoptosis-related protein expression were observed.
- Meth elevated oxidative stress markers (malondialdehyde, NADPH oxidase 4) and inflammatory factors, while decreasing antioxidants (glutathione, SOD).
Conclusions:
- Systemic administration of Meth induces significant neurotoxic effects on mouse retinas.
- The findings provide potential mechanisms for retina damage associated with Meth abuse, highlighting oxidative stress and inflammation.
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