No abstract

Complex secondary metabolites, some of which are highly toxic to mammals, are produced by many marine organisms. Some of these organisms are important food sources for marine animals and, when ingested, the toxins that they produce may be absorbed and stored in the tissues of the predators, which then become toxic to animals higher up the food chain. This is a particular problem with shellfish, and many cases of poisoning are reported in shellfish consumers each year. At present, there is no practicable means of preventing uptake of the toxins by shellfish or of removing them after harvesting. Assessment of the risk posed by such toxins is therefore required in order to determine levels that are unlikely to cause adverse effects in humans and to permit the establishment of regulatory limits in shellfish for human consumption. In the present review, the basic principles of risk assessment are described, and the progress made toward robust risk assessment of seafood toxins is discussed. While good progress has been made, it is clear that further toxicological studies are required before this goal is fully achieved.

Synthesis, characterization, antibacterial and antitumoral activities of mononuclear zinc complexes containing tridentade amine based ligands with N3 or N2O donor groups, Inorganica Chimica Acta (2014), doi: http://dx.doi.org/10.1016/j.ica. 2014.02.040 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Paralytic shellfish poisoning results from consumption of seafood naturally contaminated by saxitoxin and its congeners, the paralytic shellfish toxins (PSTs). The levels of such toxins are regulated internationally, and maximum permitted concentrations in seafood have been established in many countries. A mouse bioassay is an approved method for estimating the levels of PSTs in seafood, but this is now being superseded in many countries by instrumental methods of analysis. Such analyses provide data on the levels of many PSTs in seafood, but for risk assessment, knowledge of the relative toxicities of the congeners is required. These are expressed as “Toxicity Equivalence Factors” (TEFs). At present, TEFs are largely based on relative specific activities following intraperitoneal injection in a mouse bioassay rather than on acute toxicity determinations. A more relevant parameter for comparison would be median lethal doses via oral administration, since this is the route through which humans are exposed to PSTs. In the present study, the median lethal doses of gonyautoxin 5, gonyautoxin 6, decarbamoyl neosaxitoxin and of equilibrium mixtures of decarbamoyl gonyautoxins 2&3, C1&2 and C3&4 by oral administration to mice have been determined and compared with toxicities via intraperitoneal injection. The results indicate that the TEFs of several of these substances require revision in order to more accurately reflect the risk these toxins present to human health.

Aflatoxin concentration data for a range of foods available in New Zealand (maize products, nuts and nut products, dried fruits and spices) were combined with dietary recall food consumption information from New Zealand national nutrition surveys to derive exposure estimates for a range of age-gender groups. Mean exposure estimates for total aflatoxins ranged from 0.09-0.11 ng/kg body weight/day for adult females, to 0.32-0.39 ng/kg body weight/ day for 5-10 year old children. Spices were the major contributors to dietary exposure for all population subgroups, followed by nuts and nut products. However, the contribution of spices to total dietary exposure could be traced to a single sample with a very high concentration. A life-time weighted average aflatoxin exposure was derived for New Zealand males and females and was combined with cancer potency estimates to give an assessment of risk. The mean risk equates to a potential for less than one excess cancer every 10 years.

No abstract