The expectation is also to search for modulate, or minimize the toxic symptoms, while preserving the pro-erectile effect. Another approach, also based in this prediction model, is coming out
by using a smaller synthetic Palbociclib mouse peptide, able to mimics the action of the toxin, improving erectile function, without eliciting, or minimizing side effects. At present, our group successfully synthesized a peptide that relaxes slices of corpus cavernosum from rat and it did not show any apparent toxicity in high tested doses (100 μg) in mice. Studies are in progress to verify the mechanism of action and the real efficacy and low toxicity of this peptide and its potential use as a pro-erectile drug model. Few clinical events of priapism caused by other spiders have been reported in literature. One of them refers to a young boy who was stung by a widow spider (Latrodectus mactans) and presented priapism, along with other symptoms like prolonged pain and hypertension ( Quan and Ruha, 2009). However, it seems that see more priapism is quite uncommon in envenomation by widow spiders. Stings from all scorpions from Buthidae family,
except for Hemiscorpion ( Bawaskar and Bawaskar, 2012), may cause priapism, particularly in children ( Bahloul et al., 2010). The venom of the African scorpion Leiurus quinquestriatus quinquestriatus and the scorpion Buthus martensi Karsh relaxed rat isolated anococcygeus muscle via NO release ( Gwee et al., 1995; Srinivasan et al., 2001). However, when considering scorpions, only toxins extracted from T. serrulatus scorpion venom have been investigated as a pharmacological tool in the study of penile erection. This venom is known to act on nerve endings stimulating the 3-mercaptopyruvate sulfurtransferase release of neurotransmitters such as acetylcholine ( Gomez et al., 1973), which activate eNOS in endothelial cells. In addition, it has been demonstrated that this venom relaxes rabbit and human CC ( Teixeira et al., 1998, 2001). Nevertheless, the muscarinic receptor antagonist atropine does not affect
T. serrulatus-induced cavernosal relaxation. In both, rabbit and human CC, the typical sodium channel blocker tetrodotoxin specifically inhibited the venom-induced relaxation, suggesting the participation of sodium channels ( Teixeira et al., 1998). These authors also suggested that NO release is involved in the potentiation of erectile function by T. serrulatus venom and some of its fractions. It has been demonstrated that the toxin Ts3, from this scorpion, induces human CC relaxation, similar to that evoked by acetylcholine or electric field stimulation ( Teixeira et al., 2004a and Teixeira et al., 2004b). Ts3 binds on site 3 of the sodium channels ( Martin-Eauclaire et al., 1994) and slows-down the kinetics of inactivation ( Campos et al., 2008).