1.Synthesis, characterization and antioxidant activity of some new thiazolidin-4-one derivatives.
Apotrosoaei M, Vasincu I, Constantin S, Buron F, Routier S, Profire L. Rev Med Chir Soc Med Nat Iasi. 2014 Jan-Mar;118(1):213-8.
AIM: To design new thiazolidin-4-ones derivatives and to evaluate their potential antioxidant effects using in vitro methods.
2.New insights into the mechanism of neurolathyrism: L-β-ODAP triggers [Ca2+]i accumulation and cell death in primary motor neurons through transient receptor potential channels and metabotropic glutamate receptors.
Kusama-Eguchi K1, Miyano T2, Yamamoto M3, Suda A2, Ito Y4, Ishige K4, Ishii M5, Ogawa Y2, Watanabe K2, Ikegami F6, Kusama T7. Food Chem Toxicol. 2014 May;67:113-22. doi: 10.1016/j.fct.2014.02.021. Epub 2014 Feb 25.
Neurolathyrism is a motor neuron (MN) disease caused by β-N-oxalyl-L-α,β-diaminopropionic acid (L-β-ODAP), an AMPA receptor agonist. L-β-ODAP caused a prolonged rise of intracellular Ca(2+) ([Ca(2+)]i) in rat spinal cord MNs, and the [Ca(2+)]i accumulation was inversely proportional to the MN's life span. The [Ca(2+)]i rise induced by L-β-ODAP or (S)-AMPA was antagonized completely by NBQX, an AMPA-receptor blocker. However, blocking the L-type Ca(2+) channel with nifedipine significantly lowered [Ca(2+)]i induced by (S)-AMPA, but not that by L-β-ODAP. Tetrodotoxin completely extinguished the [Ca(2+)]i rise induced by (S)-AMPA or kainic acid, whereas that induced by L-β-ODAP was only attenuated by 65.6±6% indicating the prominent involvement of voltage-independent Ca(2+) entry. The tetrodotoxin-resistant [Ca(2+)]i induced by L-β-ODAP was blocked by 2-APB, Gd(3+), La(3+), 1-(β-[3-(4-methoxy-phenyl)propoxy]-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF-96365) and flufenamic acid, which all are blockers of the transient receptor potential (TRP) channels.
