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Journal ArticleDOI

Cellular and mitochondrial changes induced in the structure of murine skeletal muscle by crotoxin, a neurotoxic phospholipase A2 complex

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TLDR
It was concluded that the primary site of action of crotoxin was hydrolysis of the sarcolemmal membrane and that mitochondrial changes were associated with calcium accumulation in response to an altered internal environment.
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This article is published in Toxicon.The article was published on 1984-01-01. It has received 140 citations till now. The article focuses on the topics: Phospholipase A & Sarcolemma.

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Journal ArticleDOI

Excitement ahead: structure, function and mechanism of snake venom phospholipase A2 enzymes.

TL;DR: Identification of the pharmacological sites has potential for exploitation in development of novel systems useful for 'delivering' specific proteins to a particular target tissue or organ and research in this field will provide a lot of exciting opportunities.
Journal ArticleDOI

Skeletal muscle degeneration induced by venom phospholipases A2: insights into the mechanisms of local and systemic myotoxicity

TL;DR: A model is presented to explain the difference between PLA2s that induce predominantly local myonecrosis and those inducing both local and systemic myotoxicity, and the former bind not only to muscle cells, but also to other cell types, thereby precluding a systemic distribution of thesePLA2s.
OtherDOI

Mechanisms of Muscle Injury, Repair, and Regeneration

TL;DR: The process of muscle injury, repair and regeneration that occurs in muscular dystrophy is used as an example of chronic muscle injury to highlight similarities and differences between the injury and repair processes that occur in acutely and chronically injured muscle.
Journal ArticleDOI

An overview of lysine-49 phospholipase A2 myotoxins from crotalid snake venoms and their structural determinants of myotoxic action.

TL;DR: It is proposed that all the toxic activities of Lys49 PLA2s are related to their ability to destabilize natural and artificial membranes, using a cationic/hydrophobic effector site located at their C-terminal loop.
Journal ArticleDOI

Cellular pathology induced by snake venom phospholipase A2 myotoxins and neurotoxins: common aspects of their mechanisms of action

TL;DR: This work discusses how snake toxins achieve a similar cellular lesion, which is evolutionarily highly conserved, despite the differences listed above, with respect to venom PLA2s.
References
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Journal ArticleDOI

Relationship between configuration, function, and permeability in calcium-treated mitochondria.

TL;DR: The results of this work indicate that mitochondria have a built-in mechanism which responds to low levels of calcium, phosphate, and fatty acids, resulting in simultaneous changes, including increased permeability, inducation of ATPase, uncoupling of oxidative phosphorylation, and loss of respiratory control.
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A Ca2+-activated protease possibly involved in myofibrillar protein turnover. Partial characterization of the purified enzyme.

TL;DR: The purified Ca2+-activated protease (CAF) isolated from porcine skeletal muscle is optimally active on either myofibril or casein substrates at pH 7.5 and no CAF activity is detected when 1 mM Mg2+, Mn2+, Ba2+, Co2+, Ni2+, and Fe2+ are added singly, while CAF is irreversibly inhibited by iodoacetate but is unaffected by soybean trypsin inhibitor.
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Agonist-induced myopathy at the neuromuscular junction is mediated by calcium.

TL;DR: The results favor the hypothesis that esterase inhibition leads to an agonist-induced myopathy, which is mediated by Ca++ and requires an intact AChR, and could be prevented by inactivating the acetylcholine receptors with alpha- bungarotoxin or by removing Ca++ from the bath with EGTA.
Journal ArticleDOI

Role of intracellular calcium in promoting muscle damage: a strategy for controlling the dystrophic condition.

TL;DR: Suggestions are presented for different ways in which the steady-state position of [Ca2+]i might ultimately be controlled for the clinical amelioration of some dystrophic conditions.
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