DNA glycation is the DNA damage induced by reactive carbonyls (such as methylglyoxal and glyoxal) in plants and mammals. Glycation damage is quantitatively as important as oxidative damage. It is one of the major in vivo DNA damage sources associated with increased mutation frequency, DNA strand breaks, and cytotoxicity. In humans, glycation damage may contribute to Parkinson’s disease, cancer, and oxidative stress-induced diseases. Glycation damage in plant organelle (Chloroplasts and Mitochondria) DNA remains poorly understood. We recently showed that the demise of plastid DNA (ptDNA) and mitochondrial DNA (mtDNA) during maize seedling development is associated with an increase in DNA damage resulting from oxidative stress caused by reactive oxygen species. As oxidative and glycation stress are closely linked in plants, we hypothesize that glycation might be one of the causes of ptDNA and mtDNA damage during development. Glycation damage can be prevented by the activity of the protein deglycase DJ-1, also known as Parkinson's Disease Protein 7 (PARK7). Our objective is to quantify glycation lesions in the organelles of maize plant tissues in the presence and absence of DJ-1. Our approach involves the quantification of glycation and deglycation in ptDNA and mtDNA using PCR analysis and the enzyme-linked immunosorbent assay (ELISA). This research should better understand glycation damage in plant organelles and might lead to insights concerning human pathologies and neurodegenerative disease caused by glycation.

Reactive oxygen species (ROS) such as superoxide (O2–) and hydrogen peroxide (H2O2) are partially reduced oxygen molecules produced during cellular metabolism in all organisms. Plant chloroplasts and mitochondria are major ROS sources because of photosynthesis and aerobic respiration in these organelles. We previously found that the levels of oxidants were higher and antioxidants lower in maize (Zea mays) seedlings grown in the light than in the dark; these changes were accompanied by greater oxidative damage to the DNA in both chloroplasts and mitochondria in light-grown than dark-grown plants. In my research project, we will measure both H2O2 and antioxidants (catalase and peroxidase) after exposing dark-grown plants to light for increasing periods of time. Maize seedlings were grown in continuous darkness followed by 2, 4, 6, 12, and 24 hours of light. We then measured the levels of H2O2 and antioxidants in the chloroplasts and mitochondria isolated from leaf and stalk tissues during seedling development. Our data show the time course of ROS accumulation after the transfer from dark to light growth conditions and should provide a better understanding of the role of light in plant oxidative stress. Specifically, oxidative stress by ROS can be linked to DNA (mitochondria, plastid and organismal genomes) damage and by looking at the gradient of light exposure, it can open doors to discover how plants physiologically limit genetic impairment. This research can be used to assess more cancer-related topics in regards to ROS levels and how scientists can possibly find a solution in plant evolutionary-engineered genetics.