Mitochondrial activity disruption and local muscle damage induced in mice by Scolopendra polymorpha venom
Robles, Judith Tabullo De; Valverde, Francisca Fernández; Cisneros, Lucero Valladares; Villeda, Juana Hernández; Sánchez-Reyes, Ayixon; Gutiérrez, María del Carmen.
J. venom. anim. toxins incl. trop. dis;
26: e20190079, 2020. graf, ilus
Artigo
em Inglês
| LILACS
| ID: biblio-1135133
Resumo
Scolopendra polymorpha (S. polymorpha) is a predatory centipede whose venom contains a multiplicity of biochemical effectors that can cause muscle damage and cumulative cell destruction in its prey. Despite previous investigations of S. polymorpha and other centipede venoms, there is a lack of information on the morphological and biochemical patterns elicited by their myotoxic effects. To elucidate these processes, this paper presents evidence of skeletal muscle damage, and alterations in key biochemical mediators that appear only after exposure to centipede venom. Methods: Venom was collected and fractionated using RP-HPLC; mouse extensor digitorum longus (EDL) muscle was exposed to whole venom and venom fractions to evaluate myotoxicity by means of creatine kinase (CK) - a muscle damage marker - activity measurements and histochemical analysis. Results: CK activity was higher in EDL muscle exposed to venom than in unexposed muscle. This increase was observed after 15 min of venom incubation, and remained stable up to 45 min. Venom-exposed EDL muscle showed signs of muscle damage including necrosis, loss of fascicular structure as well as mitochondrial accumulations and ragged red fibers (RRF), suggesting an impairment in the normal mitochondrial arrangement. Nicotinamide adenine dinucleotide (NADH) and cytochrome oxidase (COX) tests also indicate that respiratory complexes might be affected. Conclusion: Our results suggest a different biochemical composition of S. polymorpha venom, based on the different effects of four venom fractions on the cells tested, according to statistical evidence. Fractions F6 and F7 caused the most important alterations.(AU)
Biblioteca responsável:
BR68.1
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