Triiodothyronine or Antioxidants Block the Inhibitory Effects of BDE-47 and BDE-49 on Axonal Growth in Rat Hippocampal Neuron-Glia Co-Cultures.

We previously demonstrated that polybrominated diphenyl ethers (PBDEs) inhibit the growth of axons in primary rat hippocampal neurons. Here, we test the hypothesis that PBDE effects on axonal morphogenesis are mediated by thyroid hormone and/or reactive oxygen species (ROS)-dependent mechanisms. Axonal growth and ROS were quantified in primary neuronal-glial co-cultures dissociated from neonatal rat hippocampi exposed to nM concentrations of BDE-47 or BDE-49 in the absence or presence of triiodothyronine (T3; 3-30 nM), N-acetyl-cysteine (NAC; 100 µM), or α-tocopherol (100 µM). Co-exposure to T3 or either antioxidant prevented inhibition of axonal growth in hippocampal cultures exposed to BDE-47 or BDE-49. T3 supplementation in cultures not exposed to PBDEs did not alter axonal growth. T3 did, however, prevent PBDE-induced ROS generation and alterations in mitochondrial metabolism. Collectively, our data indicate that PBDEs inhibit axonal growth via ROS-dependent mechanisms, and that T3 protects axonal growth by inhibiting PBDE-induced ROS. These observations suggest that co-exposure to endocrine disruptors that decrease TH signaling in the brain may increase vulnerability to the adverse effects of developmental PBDE exposure on axonal morphogenesis.

Hepatopathy following consumption of a commercially available blue-green algae dietary supplement in a dog.

BACKGROUND: Dietary supplement use in both human and animals to augment overall health continues to increase and represents a potential health risk due to the lack of safety regulations imposed on the manufacturers. Because there are no requirements for demonstrating safety and efficacy prior to marketing, dietary supplements may contain potentially toxic contaminants such as hepatotoxic microcystins produced by several species of blue-green algae. CASE PRESENTATION: An 11-year-old female spayed 8.95 kg Pug dog was initially presented for poor appetite, lethargy polyuria, polydipsia, and an inability to get comfortable. Markedly increased liver enzyme activities were detected with no corresponding abnormalities evident on abdominal ultrasound. A few days later the liver enzyme activities were persistently increased and the dog was coagulopathic indicating substantial liver dysfunction. The dog was hospitalized for further care consisting of oral S-adenosylmethionine, silybin, vitamin K, and ursodeoxycholic acid, as well as intravenous ampicillin sodium/sulbactam sodium, dolasetron, N-acetylcysteine, metoclopramide, and intravenous fluids. Improvement of the hepatopathy and the dog's clinical status was noted over the next three days. Assessment of the dog's diet revealed the use of a commercially available blue-green algae dietary supplement for three-and-a-half weeks prior to hospitalization. The supplement was submitted for toxicology testing and revealed the presence of hepatotoxic microcystins (MCs), MC-LR and MC-LA. Use of the supplement was discontinued and follow-up evaluation over the next few weeks revealed a complete resolution of the hepatopathy. CONCLUSIONS: To the authors' knowledge, this is the first case report of microcystin intoxication in a dog after using a commercially available blue-green algae dietary supplement. Veterinarians should recognize the potential harm that these supplements may cause and know that with intervention, recovery is possible. In addition, more prudent oversight of dietary supplement use is recommended for our companion animals to prevent adverse events/intoxications.

An outbreak of thyroid hyperplasia (goiter) with high mortality in budgerigars (Melopsittacus undulatus).

An outbreak of goiter with high morbidity and mortality in a flock of budgerigars (Melopsittacus undulatus) in California is described. Forty-five out of 400 adult birds exhibited signs of illness, weight loss, and enlargement in the crop area; 15 of the 45 birds died over a 2-3-month period. Diet consisted of a commercial mixture with the addition of broccoli, whole oats, and carrots, but no minerals or supplements. Six budgerigars were subjected to necropsy; all 6 birds had severely enlarged thyroid glands. Thyroid follicular hyperplasia was histologically observed in all birds examined, while granulomatous thyroiditis and microfollicular adenoma were observed in 2 birds, respectively. Virological, bacteriological, parasitological, and heavy metal analyses were negative or within normal limits. The total iodine in the thyroid glands of affected birds was measured by inductively coupled plasma-mass spectrometry. Following iodine supplementation and removal of broccoli from the diet, the owner reported weight gain and a reduced death rate among clinically affected birds; no additional birds became sick. The presence of broccoli with its iodine-binding ability and the complete lack of added minerals in the diet of these animals were thought to be the predisposing factors for the outbreak in the present study. Outbreaks of goiter accompanied by high mortality are rare in any species and, to the best of the authors' knowledge, have not been described previously in any avian species. Recognition of this condition may help improve medical, welfare, and trade standards concerning this species.