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ORIGINAL RESEARCH article

Front. Cell. Infect. Microbiol.
Sec. Parasite and Host
Volume 14 - 2024 | doi: 10.3389/fcimb.2024.1368019

Apigeninidin Chloride Disrupted Toxoplasma gondii Mitochondrial Membrane Potential and Induced Reactive Oxygen Species Metabolites Production

Provisionally accepted
Miya Moon Miya Moon Homa Nath Sharma Homa Nath Sharma Boakai K. Robertson Boakai K. Robertson Daniel A. Abugri Daniel A. Abugri *
  • Alabama State University, Montgomery, Alabama, United States

The final, formatted version of the article will be published soon.

    Apigeninidin chloride (APi) is a form of 3-deoxyanthrocyanidins (3-DAs) abundantly produced by the red Sorghum bicolor plant. It has been previously reported to be effective against Toxoplasma gondii (T. gondii) tachyzoites growth in vitro with less cytotoxic effect. However, its possible mechanism(s) of action has not been elucidated. Biochemically, we discovered that APi induced high reactive oxygen species (ROS) and mitochondria superoxide (MitoSOX) productions in tachyzoites leading to mitochondria membrane potential (MMP) disruption in vitro. To confirm our biochemical results at the molecular level, we performed a liquid chromatography-mass spectrometry (LC-MS) analysis on APi treated parasites to assess any metabolites and lipids alterations often associated with high ROS/MitoSOX production in cells. Noteworthy, we detected several important oxidative stress-induced metabolites such as hexanal, aldehydes, methyl undeo-10-enoate, butadiynyl phenyl ketone, 16hydroxyhexadecanoic acid (16-OH, 16:0), 2-hydroxytricosanoic acid (C23:0; O), 3-oxodecanosanoic acid (C22:1; O), 2-hydroxypropylsterate and furan fatty acids F6 (19FU-FA). These metabolites are associated with lipid, proteins and nucleic acids disruptions. Using Atovaquone (Atov) as a control, we observed that it disrupted intracellular tachyzoites mitochondrial membrane potential, increased ROS, MitoSOX production and altered metabolites and lipids production similar to what was observed with our experimental compound APi. Overall, our results indicated that APi targets T. gondii tachyzoites growth through inducing oxidative stress, mitochondrial dysfunction, and eventually parasites death.

    Keywords: 3-DAs, T. gondii, Tachyzoites, in vitro, Mitochondria membrane potential, Reactive Oxygen Species, Oxidative-stress Metabolites

    Received: 09 Jan 2024; Accepted: 26 Jun 2024.

    Copyright: © 2024 Moon, Sharma, Robertson and Abugri. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Daniel A. Abugri, Alabama State University, Montgomery, 36104, Alabama, United States

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