Photo-induced toxicity of anthracene in the Antarctic shallow water amphipod, <Emphasis Type="Italic">Gondogeneia antarctica</Emphasis>

The photo-induced toxicity of anthracene was investigated as the mortality in Antarctic shallow water amphipod, Gondogeneia antarctica, at different concentrations of anthracene and different periods of exposure to natural sunlight and artificial UVA and UVB radiations. When exposed to natural sunlight, animals contaminated in the dark and placed in clean water or in anthracene solutions showed different degrees of mortality, dose–time dependent. Effects were even more evident when these animals were exposed to artificial UVA or UVB radiations. Depuration seemed to be a slow process. The effects of UV radiation and anthracene alone and the effects of the interactions of these two stressors implied that solar radiation is an important parameter that deserves consideration in the environmental assessment of polycyclic aromatic hydrocarbons in Antarctic coastal waters. G. antarctica proved to be a good bioindicator for the phototoxicity of anthracene in Antarctic shallow waters.     

Formation and spectral characterization of Cu(II)-poly(L-ornithine) complexes.

Cu(II)-Poly-(1-ornithine) complexes in aqueous solution have been studied using potentiometric titration and absorption and circular dichroism spectra. As in the case of Cu(II)-poly(L-arginine) complexes studied previously, two types of compounds have been detected, labeled complexes I and II. Complex I contains two amine nitrogens and two water molecules coordinated to the copper. Complex II, two amine and two amide nitrogens. Amide nitrogen coordination confers optical activity to the copper d-d transitions. Furthermore, amine and amide nitrogen coordination to the copper are characterized by charge transfer transitions at 250 and 320 nm respectively which were already identified in Cu(II)-poly(L-arginine) systems.     

Honokiol ameliorates angiotensin II‐induced hypertension and endothelial dysfunction by inhibiting HDAC6‐mediated cystathionine γ‐lyase degradation

Hypertension and endothelial dysfunction are associated with various cardiovascular diseases. Hydrogen sulphide (H₂S) produced by cystathionine γ‐lyase (CSE) promotes vascular relaxation and lowers hypertension. Honokiol (HNK), a natural compound in the Magnolia plant, has been shown to retain multifunctional properties such as anti‐oxidative and anti‐inflammatory activities. However, a potential role of HNK in regulating CSE and hypertension remains largely unknown. Here, we aimed to demonstrate that HNK co‐treatment attenuated the vasoconstriction, hypertension and H₂S reduction caused by angiotensin II (AngII), a well‐established inducer of hypertension. We previously found that histone deacetylase 6 (HDAC6) mediates AngII‐induced deacetylation of CSE, which facilitates its ubiquitination and proteasomal degradation. Our current results indicated that HNK increased endothelial CSE protein levels by enhancing its stability in a sirtuin‐3‐independent manner. Notably, HNK could increase CSE acetylation levels by inhibiting HDAC6 catalytic activity, thereby blocking the AngII‐induced degradative ubiquitination of CSE. CSE acetylation and ubiquitination occurred mainly on the lysine 73 (K73) residue. Conversely, its mutant (K73R) was resistant to both acetylation and ubiquitination, exhibiting higher protein stability than that of wild‐type CSE. Collectively, our findings suggested that HNK treatment protects CSE against HDAC6‐mediated degradation and may constitute an alternative for preventing endothelial dysfunction and hypertensive disorders.