Molecular mechanism Of cell death induced by king cobra (Ophiophagus hannah) venom l-amino acid oxidase

Fung, Shin Yee; Lee, Mui Li; Tan, Nget Hong

doi:10.1016/j.toxicon.2015.01.012

Cited by 24 publications

(22 citation statements)

References 58 publications

(28 reference statements)

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“…Hemachatus + Naja venoms have a high concentration of the cytotoxic 3FTx unique to this clade [36,37,38,39,40,41,42,43,44,45]. Similarly O. hannah venoms have the highest concentration of L-amino acid oxidase of any snake venom and also the most derived forms of venom L-amino acid oxidase [23,46,47,48,49,50,51]. Taken together these results are strongly indicative of a co-evolutionary relationship between hooding behaviour and cytotoxic venom.…”

Section: Resultsmentioning

confidence: 99%

How the Cobra Got Its Flesh-Eating Venom: Cytotoxicity as a Defensive Innovation and Its Co-Evolution with Hooding, Aposematic Marking, and Spitting

Panagides

Jackson

Ikonomopoulou

et al. 2017

Toxins

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The cytotoxicity of the venom of 25 species of Old World elapid snake was tested and compared with the morphological and behavioural adaptations of hooding and spitting. We determined that, contrary to previous assumptions, the venoms of spitting species are not consistently more cytotoxic than those of closely related non-spitting species. While this correlation between spitting and non-spitting was found among African cobras, it was not present among Asian cobras. On the other hand, a consistent positive correlation was observed between cytotoxicity and utilisation of the defensive hooding display that cobras are famous for. Hooding and spitting are widely regarded as defensive adaptations, but it has hitherto been uncertain whether cytotoxicity serves a defensive purpose or is somehow useful in prey subjugation. The results of this study suggest that cytotoxicity evolved primarily as a defensive innovation and that it has co-evolved twice alongside hooding behavior: once in the Hemachatus + Naja and again independently in the king cobras (Ophiophagus). There was a significant increase of cytotoxicity in the Asian Naja linked to the evolution of bold aposematic hood markings, reinforcing the link between hooding and the evolution of defensive cytotoxic venoms. In parallel, lineages with increased cytotoxicity but lacking bold hood patterns evolved aposematic markers in the form of high contrast body banding. The results also indicate that, secondary to the evolution of venom rich in cytotoxins, spitting has evolved three times independently: once within the African Naja, once within the Asian Naja, and once in the Hemachatus genus. The evolution of cytotoxic venom thus appears to facilitate the evolution of defensive spitting behaviour. In contrast, a secondary loss of cytotoxicity and reduction of the hood occurred in the water cobra Naja annulata, which possesses streamlined neurotoxic venom similar to that of other aquatic elapid snakes (e.g., hydrophiine sea snakes). The results of this study make an important contribution to our growing understanding of the selection pressures shaping the evolution of snake venom and its constituent toxins. The data also aid in elucidating the relationship between these selection pressures and the medical impact of human snakebite in the developing world, as cytotoxic cobras cause considerable morbidity including loss-of-function injuries that result in economic and social burdens in the tropics of Asia and sub-Saharan Africa.

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Section: Resultsmentioning

confidence: 99%

How the Cobra Got Its Flesh-Eating Venom: Cytotoxicity as a Defensive Innovation and Its Co-Evolution with Hooding, Aposematic Marking, and Spitting

Panagides

Jackson

Ikonomopoulou

et al. 2017

Toxins

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“…Due to Oxy-Hb release, the ferrous (Fe 2+ ) heme was converted to ferric (Fe 3+ ) heme resulting in Met-Hb. This valence shift in Hb could be generated by oxidative stress induced by H 2 O 2 produced by the LAAO catalysis [24, 25]. Then, Hb damage could be magnified by the Met-Hb formation itself, acting as a prooxidant molecule accelerating de process of Met-Hb formation [26].…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, the newly produced arachidonic acid could be oxidized by H 2 O 2 produced by the LAAO catalysis [25]. Al Asmari et al [32] reported an increment of MDA levels in the liver, kidney, heart, and brain of mice treated with Echis pyramidum venom.…”

Section: Resultsmentioning

confidence: 99%

Rattlesnake Crotalus molossus nigrescens venom induces oxidative stress on human erythrocytes

Meléndez‐Martínez

Muñoz

Barraza-Garza

et al. 2017

J Venom Anim Toxins Incl Trop Dis

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BackgroundGlobally, snake envenomation is a well-known cause of death and morbidity. In many cases of snakebite, myonecrosis, dermonecrosis, hemorrhage and neurotoxicity are present. Some of these symptoms may be provoked by the envenomation itself, but others are secondary effects of the produced oxidative stress that enhances the damage produced by the venom toxins. The only oxidative stress effect known in blood is the change in oxidation number of Fe (from ferrous to ferric) in hemoglobin, generating methemoglobin but not in other macromolecules. Currently, the effects of the overproduction of methemoglobin derived from snake venom are not extensively recorded. Therefore, the present study aims to describe the oxidative stress induced by Crotalus molossus nigrescens venom using erythrocytes.MethodsHuman erythrocytes were washed and incubated with different Crotalus molossus nigrescens venom concentrations (0–640 μg/mL). After 24 h, the hemolytic activity was measured followed by attenuated total reflectance-Fourier transform infrared spectroscopy, non-denaturing PAGE, conjugated diene and thiobarbituric acid reactive substances determination.ResultsLow concentrations of venom (<10 μg/mL) generates oxyhemoglobin release by hemolysis, whereas higher concentrations produced a hemoglobin shift of valence, producing methemoglobin (>40 μg/mL). This substance is not degraded by proteases present in the venom. By infrared spectroscopy, starting in 80 μg/mL, we observed changes in bands that are associated with protein damage (1660 and 1540 cm−1) and lipid peroxidation (2960, 2920 and 1740 cm−1). Lipid peroxidation was confirmed by conjugated diene and thiobarbituric acid reactive substance determination, in which differences were observed between the control and erythrocytes treated with venom.Conclusions Crotalus molossus nigrescens venom provokes hemolysis and oxidative stress, which induces methemoglobin formation, loss of protein structure and lipid peroxidation.

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“…Similarly, apoxin 1, a type of LAAO from Crotalux atrox venom also induces DNA fragmentation in human umbilical endothelial cells, HL-60 (human leukaemia) A2780 (human ovarian carcinoma) and NK-3 (rat endothelial cells) due to elevated H 2 O 2 levels [81] The ACL-LAAO isolated from Agkistrodon cntortrix venom has also been demonstrated to cause DNA fragmentation in HL60 cells [30]. On the other hand, LAAO from Ophiophagus hannah venom was found to alter several apoptotic, autophagic and cell cycle-related genes, as a result of accumulated H 2 O 2 released from the enzyme action [82]. Furthermore, the LAAO also significantly up-regulates cytochrome P450 genes to further increase intracellular ROS levels [82].…”

Section: Mechanism Of Cytotoxicitymentioning

confidence: 99%

Cytotoxicity of snake venom enzymatic toxins: phospholipase A2 and l-amino acid oxidase

Hiu

Yap

2020

Biochemical Society Transactions

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The phospholipase A 2 (PLA 2 ) and L-amino acid oxidase (LAAO) are two major enzymes found in the venoms from most snake species. These enzymes have been structurally and functionally characterised for their pharmacological activities. Both PLA 2 and LAAO from different venoms demonstrate considerable cytotoxic effects on cancer cells via induction of apoptosis, cell cycle arrest and suppression of proliferation. These enzymes produce more pronounced cytotoxic effects in cancer cells than normal cells, thus they can be potential sources as chemotherapeutic agents. It is proposed that PLA 2 and LAAO contribute to an elevated oxidative stress due to their catalytic actions, for instance, the ability of PLA 2 to produce reactive oxygen species during lipolysis and formation of H 2 O 2 from LAAO catalytic activity which consequently lead to cell death. Nonetheless, the cell-death signalling pathways associated with exposure to these enzymatic toxins are not fully elucidated yet. Here in this review, we will discuss the cytotoxic effects of PLA 2 and LAAO in relationship to their catalytic mechanisms and the underlying mechanisms of cytotoxic actions.

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Molecular mechanism Of cell death induced by king cobra (Ophiophagus hannah) venom l-amino acid oxidase

Cited by 24 publications

References 58 publications

How the Cobra Got Its Flesh-Eating Venom: Cytotoxicity as a Defensive Innovation and Its Co-Evolution with Hooding, Aposematic Marking, and Spitting

How the Cobra Got Its Flesh-Eating Venom: Cytotoxicity as a Defensive Innovation and Its Co-Evolution with Hooding, Aposematic Marking, and Spitting

Rattlesnake Crotalus molossus nigrescens venom induces oxidative stress on human erythrocytes

Cytotoxicity of snake venom enzymatic toxins: phospholipase A2 and l-amino acid oxidase

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