Snake C-Type Lectins Potentially Contribute to the Prey Immobilization in Protobothrops mucrosquamatus and Trimeresurus stejnegeri Venoms

Tian, Huiwen; Liu, Ming; Li, Jiameng; Xu, Runjia; Long, Chengbo; Li, Hao; Mwangi, James; Lu, Qiumin; Lai, Ren; Shen, Chuanbin

doi:10.3390/toxins12020105

Cited by 10 publications

(7 citation statements)

References 42 publications

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“…Children may be more susceptible to stroke due to a likely higher venom-to-blood ratio in their small body relative to adults. This situation aligns more closely with the effects observed in small mammalian prey: the highly concentrated procoagulant snake toxins within a small blood volume produce a clot which travels to the brain where it is large enough to occlude a small blood vessel [ 34 , 35 , 36 , 37 ].…”

Section: Introductionsupporting

confidence: 66%

Children and Snakebite: Snake Venom Effects on Adult and Paediatric Plasma

Zdenek

Rodrigues

Bourke

et al. 2023

Toxins

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Snakebite is a globally neglected tropical disease, with coagulation disturbances being the primary pathology of many deadly snake venoms. Age-related differences in human plasma have been abundantly reported, yet the effect that these differences pose regarding snakebite is largely unknown. We tested for differences in coagulotoxic effects (via clotting time) of multiple snake venoms upon healthy human adult (18+) and paediatric (median 3.3 years old) plasma in vivo and compared these effects to the time it takes the plasmas to clot without the addition of venom (the spontaneous clotting time). We tested venoms from 15 medically significant snake species (from 13 genera) from around the world with various mechanisms of coagulotoxic actions, across the three broad categories of procoagulant, pseudo-procoagulant, and anticoagulant, to identify any differences between the two plasmas in their relative pathophysiological vulnerability to snakebite. One procoagulant venom (Daboia russelii, Russell’s Viper) produced significantly greater potency on paediatric plasma compared with adult plasma. In contrast, the two anticoagulant venoms (Pseudechis australis, Mulga Snake; and Bitis cornuta, Many-horned Adder) were significantly more potent on adult plasma. All other procoagulant venoms and all pseudo-procoagulant venoms displayed similar potency across both plasmas. Our preliminary results may inform future studies on the effect of snake venoms upon plasmas from different age demographics and hope to reduce the burden of snakebite upon society.

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Section: Introductionsupporting

confidence: 66%

Children and Snakebite: Snake Venom Effects on Adult and Paediatric Plasma

Zdenek

Rodrigues

Bourke

et al. 2023

Toxins

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“…Unfortunately, cerebral infarction or ischemic stroke is the most frequent CNS complication following viper envenoming [ 69 ] due to abnormal activation of thrombocytes, such as platelet aggregation [ 70 ]. Among the proteins in the viper venom, Snake C-type lectin-like proteins (snaclecs) are considered to be the cause of ischemic stroke by activating thrombocytes or platelets [ 71 , 72 ]. Snaclecs are mainly expressed in the venoms of vipers and colubrids [ 73 , 74 ].…”

Section: Brain Complicationsmentioning

confidence: 99%

“…Snaclecs are mainly expressed in the venoms of vipers and colubrids [ 73 , 74 ]. Regarding the vipers reported in this review, snaclecs were identified in Bothrops [ 75 , 76 ], Daboia [ 77 ], Crotalus [ 78 ], and Trimeresurus [ 71 ]. In addition, procoagulant proteases, one type of snake-venom serine proteases (SVSPs), were reported to be involved in affecting blood coagulation [ 79 , 80 ].…”

Section: Brain Complicationsmentioning

confidence: 99%

“…Toxins 2022, 14, x FOR PEER REVIEW 10 of 20 aggregation [70]. Among the proteins in the viper venom, Snake C-type lectin-like proteins (snaclecs) are considered to be the cause of ischemic stroke by activating thrombocytes or platelets [71,72]. Snaclecs are mainly expressed in the venoms of vipers and colubrids [73,74].…”

Section: Cerebral Infarction and Ischemic Strokementioning

confidence: 99%

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Cerebral Complications of Snakebite Envenoming: Case Studies

Lin

Chen

Liu

et al. 2022

Toxins

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There are an estimated 5.4 million snakebite cases every year. People with snakebite envenoming suffer from severe complications, or even death. Although some review articles cover several topics of snakebite envenoming, a review of the cases regarding cerebral complications, especially rare syndromes, is lacking. Here, we overview 35 cases of snakebite by front-fanged snakes, including Bothrops, Daboia, Cerastes, Deinagkistrodon, Trimeresurus, and Crotalus in the Viperidae family; Bungarus and Naja in the Elapidae family, and Homoroselaps (rare cases) in the Lamprophiidae family. We also review three rare cases of snakebite by rear-fanged snakes, including Oxybelis and Leptodeira in the Colubridae family. In the cases of viper bites, most patients (17/24) were diagnosed with ischemic stroke and intracranial hemorrhage, leading to six deaths. We then discuss the potential underlying molecular mechanisms that cause these complications. In cases of elapid bites, neural, cardiac, and ophthalmic disorders are the main complications. Due to the small amount of venom injection and the inability to deep bite, all the rear-fanged snakebites did not develop any severe complications. To date, antivenom (AV) is the most effective therapy for snakebite envenoming. In the six cases of viper and elapid bites that did not receive AV, three cases (two by viper and one by elapid) resulted in death. This indicates that AV treatment is the key to survival after a venomous snakebite. Lastly, we also discuss several studies of therapeutic agents against snakebite-envenoming-induced complications, which could be potential adjuvants along with AV treatment. This article organizes the diagnosis of hemotoxic and neurotoxic envenoming, which may help ER doctors determine the treatment for unidentified snakebite.

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“…The studies on TRPV1-deficit (TRPV1 KO) mice and the use of the TRPV1-specific inhibitor capsazepine suggest that TRPV1 serves as a primary nociceptor in caterpillar-induced pain. To understand the molecular mechanisms involved in the prey immobilization resulting from Protobothrops mucrosquamatus and Trimeresurus stejnegeri venoms, C-type lectin-like proteins mucetin and stejnulxin isolated from these venoms were studied [15]. It was shown that both proteins induced acute cerebral ischemia and reduced animal locomotor activity.…”

mentioning

confidence: 99%