ArticleBioMed research international2015
The effect of Walterinnesia aegyptia venom proteins on TCA cycle activity and mitochondrial NAD(+)-redox state in cultured human fibroblasts.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Effects of candesartan on cellular redox status and bioenergetics of cardiac tissue in normal and chronically stressed rats.Frontiers in pharmacology · 2026Article
- Comprehensive investigations of key mitochondrial metabolic changes in senescent human fibroblasts.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Venom of the desert black snakeToxicology research · 2021Article
- Proteomic Identification and Quantification of Snake Venom Biomarkers in Venom and Plasma Extracellular Vesicles.Toxins · 2021Article
- The effect of Echis coloratus venom on biochemical and molecular markers of the antioxidant capacity in human fibroblasts.The Libyan journal of medicine · 2017Article
- Ascorbate amelioratesExperimental and therapeutic medicine · 2017Article
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast cultures were used to study the effects of crude Walterinnesia aegyptia venom and its F1-F7 protein fractions on TCA cycle enzyme activities and mitochondrial NAD-redox state. Confluent cells were incubated with 10 μg of venom proteins for 4 hours at 37°C. The activities of all studied TCA enzymes and the non-TCA mitochondrial NADP(+)-dependent isocitrate dehydrogenase underwent significant reductions of similar magnitude (50-60% of control activity) upon incubation of cells with the crude venom and fractions F4, F5, and F7 and 60-70% for fractions F3 and F6. In addition, the crude and fractions F3-F7 venom proteins caused a drop in mitochondrial NAD(+) and NADP(+) levels equivalent to around 25% of control values. Whereas the crude and fractions F4, F5, and F7 venom proteins caused similar magnitude drops in NADH and NADPH (around 55% of control levels), fractions F3 and F6 caused a more drastic drop (60-70% of control levels) of both reduced coenzymes. Results indicate that the effects of venom proteins could be directed at the mitochondrial level and/or the rates of NAD(+) and NADP(+) biosynthesis.
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