Marine environment has demonstrated to be an interesting source of compounds with uncommon and unique chemical features on which the molecular modeling and chemical synthesis of new drugs can be based with greater efficacy and specificity for the therapeutics. Cancer is a growing public health threat, and despite the advances in biomedical research and technology, there is an urgent need for the development of new anticancer drugs. In this field, it is estimated that more than 60% of commercially available anticancer drugs are natural biomimetic inspired. Among the marine organisms, algae have revealed to be one of the major sources of new compounds of marine origin, including those exhibiting antitumor and cytotoxic potential. These compounds demonstrated ability to mediate specific inhibitory activities on a number of key cellular processes, including apoptosis pathways, angiogenesis, migration and invasion, in both in vitro and in vivo models, revealing their potential to be used as anticancer drugs. This review will focus on the bioactive molecules from algae with antitumor potential, from their origin to their potential uses, with special emphasis to the alga Sphaerococcus coronopifolius as a producer of cytotoxic compounds.

Chitin was extracted from Polybius henslowii, a swimming crab, captured in large quantities throughout the Portuguese coast by purse seine vessels as bycatch. After standard chitin extraction procedures, water-soluble chitosan products were obtained via two different methods: (1) N-acetylation with the addition of acetic anhydride and (2) a reaction with hydrogen peroxide. The chemical structure and molecular weight of chitosan derivatives, water-soluble chitosan (WSC) and chitooligosaccharides (COS), were confirmed by Fourier Transform Infrared Spectroscopy (FT-IR) and gel permeation chromatography (GPC). Antioxidant and metal chelation activities were evaluated, and the growth inhibition capacity was tested on four phytopatogens. The chitooligosaccharides from pereopods (pCOS) and shell body parts (sCOS) inhibited all fungal species tested, particularly Cryphonectria parasitica with 84.7% and 85.5%, respectively. Both radical scavenging and antifungal activities proved to be dose-dependent. Chitooligosaccharides with a low molecular weight (2.7, 7.4, and 10.4 Kg·mol⁻¹) showed the highest activity among all properties tested. These results suggested that chitosan derivatives from P. henslowii raw material could potentially be used against phytopathogens or as ingredient in cosmetics and other products related to oxidative stress.

The present study was designed to evaluate the nature of intervening agents in L‐DOPA‐ and dopamine‐induced neurotoxicity in Neuro‐2A cells. In the absence of cells and in conditions of light protection, at 37°C, L‐DOPA or dopamine (1 mM) in culture medium degraded spontaneously in a time‐dependent manner, this being prevented by ascorbic acid (200 μM) and other antioxidants, namely glutathione (1 mM), N‐acetyl‐L‐cysteine (1 mM), sodium metabisulphite (200 μM), but not N‐ter‐butyl‐α‐phenylnitrone (1 mM) and deferoxamine (100 μM). The viability of Neuro‐2A cells declined following treatment with L‐DOPA or dopamine in a concentration‐ and time‐dependent manner. The decrease in cell viability by L‐DOPA (10±4% of control) or dopamine (15±4% of control) was markedly attenuated by antioxidants (ascorbic acid, glutathione, N‐acetyl‐L‐cysteine and sodium metabisulphite). Autoxidation of L‐DOPA or dopamine was accompanied by the formation of H₂O₂ in a time‐dependent manner, this being completely prevented by ascorbic acid at 24 h or markedly reduced at 48 h. Protective effects of 100 U ml⁻¹ catalase (40±1% of control) against L‐DOPA‐induced cell death were lower than those conferred by 200 μM ascorbic acid (70±3% of control). Catalase‐induced protection (59±5% of control) against dopamine‐induced cell death was similar to that conferred by 200 μM ascorbic acid (57±4% of control). L‐DOPA‐induced neuronal cell death was also accompanied by increases in caspase‐3 activity, this being insensitive to ascorbic acid. Dopamine‐induced increase in caspase‐3 activity occurred only when autoxidation of the amine was prevented by ascorbic acid. It is suggested that in addition to generation of H₂O₂ and quinone formation, L‐DOPA‐ and dopamine‐induced cell death may result from induction of apoptosis, as evidenced by increases in caspase‐3 activity. Dopamine per se induces apoptosis by a mechanism independent of oxidative stress, as evidenced by the fact that increases in caspase‐3 activity occurred only when autoxidation of the amine was prevented. British Journal of Pharmacology (2002) 137, 1305–1313. doi:10.1038/sj.bjp.0704982