Journal
TOXICOLOGY LETTERS
Volume 289, Issue -, Pages 99-106Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2018.02.001
Keywords
D-galactose; Premature senescence; Autophagy flux; Oxidative stress; Mitochondrial dysfunction
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Funding
- National Natural Science Foundation of China [81673710]
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Cataract is the leading cause of blindness with an estimated 16 million people affected worldwide. D-galactose (D-gal) is a reducing sugar that widely distributed in foodstuffs, and studies show that D-gal could promote cataract formation by damaging nature lens epithelial cells (LECs). However, the underlying mechanism is unclear. In our present study, D-gal resulted in premature senescence of LECs, which was confirmed by determining the ss-galactosidase activity, cell proliferative potential and cell cycle distribution, though apoptosis of LECs was not observed. We also verified that D-gal induced the impairment of autophagy flux by measuring the expression of LC3II and P62. Meanwhile, we found that D-gal induced mitochondrial dysfunctions of LECs through increasing reactive oxygen species (ROS), reducing ATP synthesis and mitochondrial potential (MMP), enhancing the concentration of cytoplasm Ca2+ and permeability transition pore (mPTP) opening. Metformin, as a potential anti-aging agent, suppressed the senescence of LECs by restoring autophagy flux and mitochondria functions. Nevertheless, the antioxidant N-acetylcysteine (NAC) scavenged ROS significantly but was not efficient in preventing LECs from premature senescence. Our data suggests that restoring autophagy activity and improving mitochondrial functions may be a potential strategy for the prevention of LECs senescence-related cataract.
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