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1.
Mar Drugs ; 17(10)2019 Oct 10.
Article in English | MEDLINE | ID: mdl-31658661

ABSTRACT

Prasiola crispa is a macroscopic green algae found in abundance in Antarctica ice free areas. Prasiola crispan-hexaneextract (HPC) induced insecticidal activity in Nauphoeta cinerea cockroaches after 24 h of exposure. The chemical analysis of HPC revealed the presence of the followingphytosterols: ß-sitosterol, campesterol and stigmasterol. The incubation of cockroach semi-isolated heart preparations with HPC caused a significant negative chronotropic activity in the heartbeats. HPC affected the insect neuromuscular function by inducing a complete inhibition of the cockroach leg-muscle twitch tension. When the isolated phytosterols were injected at in vivo cockroach neuromuscular preparations, there was a progressive inhibition of muscle twitches on the following order of potency: ß-sitosterol > campesterol > stigmasterol. HPC also provoked significant behavioral alterations, characterized by the increase or decrease of cockroach grooming activity, depending on the dose assayed. Altogether, the results presented here corroborate the insecticide potential of Prasiola crispa Antarctic algae. They also revealed the presence of phytosterols and the involvement of these steroidal compounds in the entomotoxic activity of the algae, potentially by modulating octopaminergic-cholinergic pathways. Further phytochemical-combined bioguided analysis of the HPC will unveil novel bioactive compounds that might be an accessory to the insecticide activity of the algae.


Subject(s)
Chlorophyta/chemistry , Cockroaches , Insecticides/chemistry , Phytosterols/analysis , Plant Extracts/chemistry , Animals , Antarctic Regions , Hexanes/chemistry , Insecticides/isolation & purification , Lethal Dose 50 , Plant Extracts/isolation & purification
3.
Neurotoxicology ; 65: 264-271, 2018 03.
Article in English | MEDLINE | ID: mdl-29174112

ABSTRACT

The biological activity of Rhinella icterica toxic secretion (RITS) was evaluated on chick neuromuscular junctions, rat heart́s tissue and mice hippocampal slices. At chick biventer cervicis preparation, RITS (5, 10 and 20µg/mL) produced a concentration-independent irreversible neuromuscular blockade, which was preceded by a transitory increase of muscle twitch tension with the lowest concentration, in 120min recordings. In this set of experiments, RITS incubation partially prevented the curare neuromuscular blockade. The assessment of chick biventer cervicis muscle acetylcholinesterase (AChE) in the presence of RITS showed a significant inhibition of the enzyme, similarly to neostigmine. The incubation of muscles with digoxin or ouabain mimicked the poison activity by increasing the amplitude of the twitches followed by a progressive depression of the muscle strength. In addition, RITS demonstrated a digitalic-like activity, by inhibiting significantly the cardiac Na+, K+-ATPase. When the central nervous system was accessed, RITS induced an increase in the cell viability, in the lowest concentration. In addition, the poison protected slices subject to oxygen/glucose deprivation. Altogether, these data indicate that the poisonous extract of R. icterica is able to interfere with peripheral and central neurotransmission, probably due to a direct interaction with AChE, calcium channels and Na+, K+-ATPase. A further investigation upon the poison toxic components will unveil the components involved in such a pharmacological activity and the potential biotechnological application of this poison.


Subject(s)
Amphibian Venoms/toxicity , Bufonidae , Hippocampus/drug effects , Myocardium/metabolism , Neuromuscular Junction/drug effects , Animals , Cell Survival/drug effects , Chickens , Cholinesterase Inhibitors/toxicity , Curare/antagonists & inhibitors , Curare/pharmacology , Digoxin/pharmacology , Dose-Response Relationship, Drug , Ischemia/prevention & control , Male , Mice , Neuromuscular Blocking Agents/pharmacology , Neuromuscular Junction/metabolism , Ouabain/pharmacology , Rats , Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors
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