Inhibiting Effect of Zinc Oxide Nanoparticles on Advanced Glycation Products and Oxidative Modifications: a Potential Tool to Counteract Oxidative Stress in Neurodegenerative Diseases Jalaluddin M. Ashraf 1 & Mohammad Azam Ansari 2 & Sana Fatma 3 & Saleh M. S. Abdullah 1 & Johar Iqbal 4 & Aymen Madkhali 1 & Al Hassan Hamali 1 & Saheem Ahmad 5 & Ahmed Jerah 1 & Valentina Echeverria 6 & George E. Barreto 7 & Ghulam Md Ashraf 8 Received: 20 November 2017 /Accepted: 25 January 2018 # Springer Science+Business Media, LLC, part of Springer Nature 2018 Abstract Advanced glycation end products (AGEs) are implicated in several central nervous system (CNS) pathologies including Alzheimer and Parkinson’ s diseases. In the face-off of AGE menace, we have attempted to investigate the zinc oxide nanoparticle (ZnONP) role in inhibition of AGE formation. Synthesized ZnONPs were used to investigate the inhibitory effects on AGE formation. The inhibitory effects of ZnONPs on AGE formation were determined by biophysical immunological and biochem- ical techniques. The results showed that ZnONP is a potential anti-glycating agent inhibiting AGE formation as well as protecting the protein structure from change. Therefore, our findings suggest ZnONPs may be used as a therapeutic in resolving the AGE role in CNS-related complications. Keywords Advanced glycation end products . Anti-glycating agent . Neurodegenerative diseases . Nanoparticles Introduction The non-enzymatic glycation named Maillard reaction is an unavoidable phenomenon even under physiological condition resulting in advanced glycation end products (AGEs). It is now well established that long-term exposure of macromole- cules during metabolic dysfunction and/or other diseased con- ditions (specifically neurodegenerative events) drastically in- creases non-enzymatic glycation reaction and eventually leads to AGE accumulation [1–4]. Increasing evidence suggests that excessive formation of oxidative stress and accumulation of AGEs in the body result in oxidative and carbonyl stress, in- flammation, and structural and functional changes of tissue proteins, as a consequence of Alzheimer’ s disease (AD) and Parkinson’ s disease (PD) [1, 5]. Previously, it was considered that only reducing sugars were involved in glycation reaction, i.e., AGE formation, but later, several other non-sugar compounds were also reported to be indulged in glycation reactions [6, 7]. α-Dicarbonyl species (methylglyoxal (MG), glyoxal (G), and 3-deoxyglucosone Jalaluddin M. Ashraf and Mohammad Azam Ansari are equally contributing authors * Jalaluddin M. Ashraf jmashraf@gmail.com * Mohammad Azam Ansari azammicro@gmail.com; maansari@iau.edu.sa * Ghulam Md Ashraf ashraf.gm@gmail.com 1 Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia 2 Department of Epidemic Disease Research, Institute of Research and Medical Consultations (IRMC), Imam Abdulrahman Bin Faisal University, Dammam 31441, Saudi Arabia 3 Institute of Science, Banaras Hindu University, Varanasi, India 4 Faculty of Medicine, Jazan University, Jazan, Saudi Arabia 5 Department of Biosciences, Integral University, Lucknow, India 6 Facultad de Ciencias de la Salud, Universidad San Sebastián, Lientur 1457, 4030000 Concepción, Chile 7 Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia 8 King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia Molecular Neurobiology https://doi.org/10.1007/s12035-018-0935-x