How Well Does Australian Animal Welfare Policy Reflect Scientific Evidence: A Case Study Approach Based on Lamb Marking.

The development and substance of animal welfare policy is subject to a range of social, cultural, economic, and scientific influences that commonly vary within and between countries. Discrepancies in policy can create confusion and mistrust among stakeholders and consumers and limit the ability to create a uniform minimum level of requirements to safeguard animal welfare, as well as create a level 'playing field' for farmers when trading with other jurisdictions. The livestock sector is receiving growing scrutiny globally for real and perceived violations of animal welfare, for example, the practice of mulesing in Australia.

Characterization of non-radiolabeled Thyroxine (T) uptake in cryopreserved rat hepatocyte suspensions: Pharmacokinetic implications for PFOA and PFOS chemical exposure.

The alteration of thyroxine (T) cellular uptake by an environmental chemical can serve as a contributing factor in thyroid hormone (TH) disruption. Herein, we describe a non-radiolabeled (LC-MS/MS) oil-filtration technique designed to characterize the mechanism(s) responsible for T cellular uptake in cryopreserved rat hepatocyte suspensions. The environmental chemicals perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) were evaluated for their effect on T hepatic uptake.

In vitro metabolism of thyroxine by rat and human hepatocytes.

1. The liver metabolizes thyroxine (T(4)) through two major pathways: deiodination and conjugation. Following exposure to xenobiotics, T(4) conjugation increases through the induction of hepatic uridine diphosphate glucuronosyltransferase (UGT) in rodents; however, it is uncertain to what degree different species employ deiodination and conjugation in the metabolism of T(4).

Effects of perinatal PBDE exposure on hepatic phase I, phase II, phase III, and deiodinase 1 gene expression involved in thyroid hormone metabolism in male rat pups.

Previous studies demonstrated that perinatal exposure to polybrominated diphenyl ethers (PBDEs), a major class of brominated flame retardants, may affect thyroid hormone (TH) concentrations by inducing hepatic uridinediphosphate-glucoronosyltransferases (UGTs). This study further examines effects of the commercial penta mixture, DE-71, on genes related to TH metabolism at different developmental time points in male rats. DE-71 is predominately composed of PBDE congeners 47, 99, 100, 153, 154 with low levels of brominated dioxin and dibenzofuran contaminants.

Comparative absorption and bioaccumulation of polybrominated diphenyl ethers following ingestion via dust and oil in male rats.

Household dust has been implicated as a major source of polybrominated diphenyl ether (PBDE) exposure in humans. This finding has important implications for young children, who tend to ingest more dust than adults and may be more susceptible to some of the putative developmental effects of PBDEs. Absorption parameters of PBDEs from ingested dust are unknown; therefore, the objectives of this study were to determine and to compare the uptake of PBDEs from either household dust (NIST Standard Reference Material 2585) or a corn oil solution.

Possible mechanisms of thyroid hormone disruption in mice by BDE 47, a major polybrominated diphenyl ether congener.

Polybrominated diphenyl ethers (PBDEs) are a class of polyhalogenated aromatic compounds commercially used as fire retardants in consumer products. These compounds have been shown to decrease thyroid hormone concentrations in rodents after acute exposures. This study examines the ability of 2,2',4,4'-tetrabromodiphenyl ether (BDE 47) to decrease circulating thyroid hormone concentrations and pairs this with BDE 47-induced effects on genes involved in thyroid hormone homeostasis.