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Journal Article

Citation

Sitprija V, Sitprija S. Toxicon 2019; 161: 44-49.

Affiliation

Department of Biology, Mahidol University, Rama 6 Road, Bangkok 10400, Thailand. Electronic address: siravit.sit@mahidol.ac.th.

Copyright

(Copyright © 2019, Elsevier Publishing)

DOI

10.1016/j.toxicon.2019.02.012

PMID

30826470

Abstract

Marine toxins are known among several causes of toxin induced renal injury. Enzymatic mechanism by phospholipase A2 is responsible for acute kidney injury (AKI) in sea snake envenoming without any change in cardiac output and systemic vascular resistance. Cnidarian toxins form pores in the cell membrane with Ca influx storm resulting in cell death. Among plankton toxins domoic acid, palytoxin and maitotoxin cause renal injury by ion transport into the cell through ion channels resulting in renal cell swelling and lysis. Okadaic acid, calyculin A, microcystin LR and nodularin cause AKI by serine threonine phosphatase inhibition and hyperphosphorylation with increased activity of Ca2+/calmodulin - dependent protein kinase II, increased cytosolic Ca2+, reactive oxygen species, caspase and P53. Renal injury by plankons is mostly subclinical and requires sensitive biomarker for diagnosis. In this respect repeated consumption of plankton toxin contaminated seafood is a risk of developing chronic renal disease. The subject deserves more clinical study and scientific attention.

Copyright © 2019. Published by Elsevier Ltd.


Language: en

Keywords

Marine toxins; PLA(2); cnidarian; plankton; protein phosphatase inhibitor; renal injury; sea snake

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