Effects of malathion and carbendazim on Amazonian freshwater organisms: comparison of tropical and temperate species sensitivity distributions

The risk assessment of pesticides for freshwater ecosystems in the Amazon has relied on the use of toxicity data and water quality criteria derived for temperate regions due to a lack of ecotoxicological studies performed with indigenous species. This leaves an unknown margin of uncertainty for the protection of Amazonian ecosystems, as differences in environmental conditions and species sensitivity are not taken into account. To address this issue, the acute toxic effects of malathion (an organophosphorus insecticide) and carbendazim (a benzimidazole fungicide) were assessed on five fish and five freshwater invertebrates endemic to the Amazonian region. Subsequently, the intrinsic sensitivity of Amazonian and temperate freshwater species was compared using the species sensitivity distribution (SSD) concept. Amazonian species sensitivity to malathion was found to be similar to that of their temperate counterparts, with LC50 values ranging between 111 and 1507 μg/l for fish species and 2.1–426 μg/l for arthropod species. However, Amazonian fish appeared to be slightly less sensitive for carbendazim than temperate fish with LC50 values ranging between 1648 and 4238 μg/l, and Amazonian invertebrates were found to be significantly more resistant than their temperate counterparts, with LC50 values higher than 16000 μg/l. The results of this study suggest that for these compounds, the use of water quality criteria derived with laboratory toxicity data for temperate species will result in a sufficient protection level for Amazonian freshwater organisms. Recommendations for further research include the validation of threshold concentrations derived with temperate standard test species and with the SSD model with semi-field experiments considering larger assemblages of indigenous species under local environmental conditions

Vitamin C and the common cold: a retrospective analysis of Chalmers’ review.

In 1975 Thomas Chalmers analyzed the possible effect of vitamin C on the common cold by calculating the average difference in the duration of cold episodes in vitamin C and control groups in seven placebo-controlled studies. He found that episodes were 0.11 +/- 0.24 (SE) days shorter in the vitamin C groups and concluded that there was no valid evidence to indicate that vitamin C is beneficial in the treatment of the common cold. Chalmers' review has been extensively cited in scientific articles and monographs. However, other reviewers have concluded that vitamin C significantly alleviates the symptoms of the common cold. A careful analysis of Chalmers' review reveals serious shortcomings. For example, Chalmers did not consider the amount of vitamin C used in the studies and included in his meta-analysis was a study in which only 0.025-0.05 g/day of vitamin C was administered to the test subjects. For some studies Chalmers used values that are inconsistent with the original published results. Using data from the same studies, we calculated that vitamin C (1-6 g/day) decreased the duration of the cold episodes by 0.93 +/- 0.22 (SE) days; the relative decrease in the episode duration was 21%. The current notion that vitamin C has no effect on the common cold seems to be based in large part on a faulty review written two decades ago

Dental caries in rats associated with Candida albicans

In addition to occasional opportunistic colonization of the oral mucosa, Candida albicans is frequently found in carious dentin. The yeast's potential to induce dental caries as a consequence of its pronounced ability to produce and tolerate acids was investigated. Eighty caries-active Osborne-Mendel rats were raised on an ampicillin-supplemented diet and exposed to C. albicans and/or Streptococcus mutans, except for controls. Throughout the 28-day test period, the animals were offered the modified cariogenic diet 2000a, containing 40% various sugars. Subsequently, maxillary molars were scored for plaque extent. After dissection, the mandibular molars were evaluated for smooth surface and fissure caries. Test animals exposed to C. albicans displayed considerably more advanced fissure lesions (p < 0.001) than non-exposed controls. While S. mutans yielded similar results, a combined association of C. albicans and S. mutans had no effect on occlusal caries incidence. Substituting dietary sucrose by glucose did not modify caries induction by C. albicans. However, animals fed a diet containing 20% of both sugars showed no differences to non-infected controls. Smooth surface caries was not generated by the yeast. This study provides experimental evidence that C. albicans is capable of causing occlusal caries in rats at a high rate

Enteral Feeding Reduces Endothelial Nitric Oxide Synthase in the Caudal Intestinal Microvasculature of Preterm Piglets.

The initiation of enteral feeding represents a challenge to the neonatal intestinal microcirculation, especially in preterms where it predisposes to necrotizing enterocolitis (NEC). We hypothesized that a structural microvascular deficiency may occur when enteral feeding is initiated in preterm piglets susceptible to NEC. Stereologic volume densities of a pan-endothelial marker (vWF), and the main vasodilator endothelial nitric oxide synthase (eNOS), were determined along the small intestine of 1) unfed preterm piglets, 2) piglets receiving total parenteral nutrition (TPN) for 2-3 d, and 3) piglets fed 2 d sow's colostrum (TPN+SOW) or milk formula (TPN+FOR) following TPN. In the mucosa, vWF-density decreased in a cranio-caudal direction. A corresponding mucosal eNOS gradient appeared only after initiating enteral feeding. In TPN+SOW, eNOS induction may lag behind the mucosal growth of the caudal region. In TPN+FOR, formula-related factors (i.e. bacteria, cytokines) may suppress mucosal eNOS, indicated by increased stress-sensitive nuclear HIF1alpha staining. The low mucosal endothelial eNOS density was related to the presence of NEC lesions, maybe via increased hypoxia-sensitivity, especially in the caudal region as indicated by nuclear HIF1alpha-staining. Our results suggest an insufficient structural adaptation of the microvasculature to enteral feeding, especially of mucosal eNOS, which may lead to NEC. AD - Department of Veterinary Medicine [E.R.H, M.O., A.L.M.W., C.J.G.], University of Antwerp, 2610 Wilrijk, Belgium; Department of Human Nutrition [T.T., P.T.S.], University of Copenhagen, Frederiksberg DK-1958, Denmark; Department of Pharmacology, Toxicology, Biochemistry and Organ Physiology [S.U.S.], University of Ghent, 9820 Merelbeke, Belgium; Department of Anatomy and Embryology [W.H.L.], University of Maastricht, 6200 MD Maastricht, The Netherlands