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BACKGROUND Potato tubers from genetically modified plants overexpressing the StDREB1 or the VvWRKY2 transcription factors that exhibited improved tolerance to salt and resistance to Fusarium solani infection were characterized and evaluated for safety in a 30 day rat feeding study. Male Wistar rats were split into four groups and provided with a diet composed of 33% (w/w) of either one of the two genetically modified potatoes (GMPs), 33% of the commercial Spunta variety (Sp), or a control group fed with the basal rats' diet. The influence of the GMPs on rat behavior and overall health parameters was evaluated and compared with that of commercial potato (i.e. the Sp group) and control diet. RESULTS Small differences were noticed in the chemical composition of the different tubers, but all the diets were adjusted to an identical caloric level. Results showed no sign of toxic or detrimental effects on the rats' overall health as a result of these diets. The rats fed with the GMPs meal showed hematological and biochemical compositions of the plasma comparable to the control groups. No histopathological damage nor any structural disorganization, severe congestion, or acute inflammation were noticed in the rats' tissues. CONCLUSION Under these study conditions, the GMP diets did not induce any apparent or significant adverse effects on rats after 30 days of dietary administration in comparison with rats fed diets with the corresponding non‐transgenic diet and the standard diet group. These two GMPs were therefore considered to be as safe as their commercial comparator. © 2022 Society of Chemical Industry.

The redox status is determined by the balance between the production of reactive oxygen species (ROS) and their removal by the antioxidant defense system. Mitochondria, the center of oxidative metabolism and the principal site of ROS production, are crucial in health and also in the pathogenesis of many diseases. Mitochondrial dysfunction, resulting in a vicious cycle contributing to cellular damage and consequent cell death, has been proven to play a critical role in the pathogenesis of cardiovascular diseases. Previous studies have shown that mitochondrial transfer in cells plays a crucial role in regulating cardiovascular system development and maintaining normal tissue homeostasis. We review and evaluate in this chapter the evidence for mitochondrial dysfunction as a consequence of stress exposure and a contributing factor to cardiovascular diseases.