Subchronic toxicity of Baltic herring oil and its fractions in the rat II: Clinical observations and toxicological parameters

This study aimed to increase the knowledge about the toxicity of fish-derived organohalogen pollutants in mammals. The strategy chosen was to separate organohalogen pollutants derived from Baltic herring (Clupea harengus) fillet, in order to obtain fractions with differing proportions of identified and unidentified halogenated pollutants, and to perform a subchronic toxicity study in rats, essentially according to the OECD guidelines, at three dose levels. Nordic Sea Iodda (Mallotus villosus) oil, with low levels of persistent organohalogen pollutants, was used as an additional control diet. The toxicological examination showed that exposure to Baltic herring oil and its fractions at dose levels corresponding to a human intake in the range of 1.6 to 34.4 kg Baltic herring per week resulted in minimal effects. The spectrum of effects was similar to that, which is observed after low-level exposure to pollutants such as chlorinated dibenzo-p-dioxins and dibenzofurans (CDD/F) and chlorinated biphenyls, despite the fact that these contaminants contribute to a minor part of the extractable organically bound chlorine (EOC1). The study confirmed previous findings that induction of hepatic ethoxyresorufin deethylase (EROD) activity takes place at daily intake levels 0.15 ng fish-derived CDD/F-TEQs/kg body weight. The study also demonstrated that hepatic vitamin A reduction takes place at somewhat higher daily exposure levels, i.e. 0.16-0.30 ng fish-derived CDD/F-TEQs/kg body weight. Halogenated fatty acids, the major component of EOC1, could not be linked to any of the measured effects. From a risk management point of view, the study provides important new information of effect levels for Ah-receptor mediated responses following low level exposure to organohalogen compounds from a matrix relevant for human exposure

Acaricidal effects of Corymbia citriodora oil containing para-menthane-3,8-diol against nymphs of Ixodes ricinus (Acari: Ixodidae)

The toxicity of para-menthane-3,8-diol (PMD), the main arthropod-repellent compound in the oil of the lemon eucalyptus, Corymbia citriodora, was evaluated against nymphs of Ixodes ricinus using five methods (A-E) of a contact toxicity bioassay. Mortality rates were estimated by recording numbers of dead nymphs at 30 min intervals during the first 5 h after the start of exposure and at longer intervals thereafter. The mortality rate increased with increasing concentration of PMD and duration of exposure with a distinct effect after 3.5 h. From the results obtained by methods A, C and E, the LC(50) range was 0.035-0.037 mg PMD/cm(2) and the LC(95) range was 0.095-0.097 mg PMD/cm(2) at 4 h of exposure; the LT(50) range was 2.1-2.8 h and the LT(95) range was 3.9-4.2 h at 0.1 mg PMD/cm(2). To determine the duration of toxic activity of PMD, different concentrations (0.002, 0.01, 0.1 mg PMD/cm(2)) were tested and mortality was recorded at each concentration after 1 h; thereafter new ticks were tested. This test revealed that the lethal activity of PMD remained for 24 h but appeared absent after 48 h. The overall results show that PMD is toxic to nymphs of I. ricinus and may be useful for tick control

Acaricidal properties of ylang-ylang oil and star anise oil against nymphs of Ixodes ricinus (Acari: Ixodidae)

Ylang-ylang oil (YYO) from Cananga odorata (Lam.) Hook.f. & Thomson and star anise oil (SAO) from Illicium verum Hook.f. were tested at four concentrations 0.05, 0.1, 0.2, 0.4 mu l/cm(2). Mortality rates were obtained by counting dead nymphs at 30-min intervals during the first 5h after the start of exposure and then at 24, 48 and 72h. Mortality increased with increasing oil concentration and time of exposure. The two highest concentrations of YYO (0.2, 0.4 mu l/cm(2)) gave maximum lethal concentrations (LC) of 50 and 95% mortality after 4.5h exposure. Mortality of 95% was obtained after 24h with the next highest dose (0.1 mu l/cm(2)), whereas LC95 required 3days with the lowest YYO (0.05 mu l/cm(2)). The lethal effect time (LT) was correlated with the duration of exposure, with a significant effect at 0.4l YYO/cm(2) after 3h' (LT50=3.2h, LT95=4.3h). In contrast, only the highest concentration of SAO, 0.4 mu l SAO/cm(2), showed increasing mortality with time of exposure. This reached LT50 after 10h and LT95 after 24h. However, with the lower concentration (0.2 mu l/cm(2)) 50% mortality was reached after 24h and 100% at 72h. At to the lowest concentration of SAO (0.1 mu l/cm(2)), 67% mortality after 48h. The study indicates that YYO and SAO exhibit strong acaricidal properties against nymphs of I. ricinus and suggest that both YYO and SAO should be evaluated as potentially useful in the control of ticks

Effects of gastrin on calcium homeostasis in chickens

As in the rat, gastrin and an extract of the acid-producing part of the stomach (proventriculus) were found to lower the blood Ca2+ concentration in the chicken. Furthermore, gastrin enhanced the uptake of 45Ca into the femur. It has been suggested previously that gastrin causes hypocalcemia in the rat by releasing gastrocalcin, a hypothetical hormone thought to reside in the acid-producing part of the stomach. The results of the present study in the chicken are in agreement with this concept. Not only exogenous, but also endogenous gastrin lowered blood calcium levels. Thus, the serum gastrin concentration was increased in response to ranitidine-evoked blockade of the gastric acid output; the rise in gastrin was associated with a transient drop in blood calcium. Also, food intake produced a rise in the serum gastrin concentration and a transient drop in blood calcium. However, injection of ranitidine or food intake in proventriclectomized (acid-producing part of the stomach extirpated) chickens failed to lower blood calcium, supporting the view that the gastrin-evoked hypocalcemia depends upon an agent in the gastric (proventriculus) mucosa. We suggest that endogenous and exogenous gastrin evoke hypocalcemia in the chicken by the same mechanism as that which has been postulated in the rat, i.e. by mobilization of the candidate hormone gastrocalcin from endocrine cells in the acid-producing gastric mucosa