Effect of thyroidectomy and thyroxine on hexachlorobenzene induced porphyria.

J Endocrinol Invest

Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Argentina.

Published: May 1994

AI Article Synopsis

  • The study investigated how thyroid hormone levels affect porphyria caused by hexachlorobenzene (HCB) in different groups of rats.
  • After 8 days of HCB exposure, serum T4 levels dropped in rats, but T3 levels remained unchanged.
  • The results indicated that thyroid hormone is crucial in the early onset of HCB-induced porphyria, with T4-treated rats showing a quicker decrease in PCL activity compared to normal and thyroidectomized rats.

Article Abstract

The role of thyroid status in hexachlorobenzene (HBC) induced porphyria was studied in normal, thyroidectomized and thyroxine (T4) treated rats. Female Wistar rats were treated with HCB for different periods of time. Serum T4 levels were depressed after 8 days of HCB administration whereas levels of triiodothyronine (T3) were not altered. T4 administered simultaneously with HCB resulted in hyperthyroxinemia. The time course of porphyrinogen carboxy-lyase (PCL) activity in the three HBC treated groups was studied. A rapid and significant decrease of PCL activity was found after 8 days of HCB treatment in T4 treated rats with respect to untreated animals. In contrast, HCB treatment of normal and thyroidectomized rats elicited a significant decrease of PCL activity after 21 and 30 days, respectively. This study shows that thyroid hormone plays an important role in the early establishment of HCB induced porphyria.

Download full-text PDF

Source
http://dx.doi.org/10.1007/BF03348984DOI Listing

Publication Analysis

Top Keywords

induced porphyria
12
pcl activity
12
normal thyroidectomized
8
treated rats
8
days hcb
8
decrease pcl
8
activity days
8
hcb treatment
8
hcb
6
thyroidectomy thyroxine
4

Similar Publications

Background: Rho-associated kinases 1 and 2 (ROCK1 and ROCK2) regulate critical cell functions, including actomyosin contractility, apoptosis, and proliferation. Some studies suggest that ROCK inhibition may serve as a treatment for liver fibrosis. More investigation is needed to understand the role of hepatocyte ROCK signaling in vivo, especially in the context of profibrotic liver injury.

View Article and Find Full Text PDF

The histamine pathway is a target to treat hepatic experimental erythropoietic protoporphyria.

Cell Mol Gastroenterol Hepatol

January 2025

Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ, USA. Electronic address:

Background & Aims: Erythropoietic protoporphyria (EPP) is caused by mutations in ferrochelatase which inserts iron into protoporphyrin-IX (PP-IX) to generate heme. EPP is characterized by PP-IX accumulation, skin photosensitivity, cholestasis, and end-stage liver disease. Despite available drugs that address photosensitivity, treatment of EPP-related liver disease remains an unmet need.

View Article and Find Full Text PDF

Erythropoietic protoporphyria (EPP1) results in painful photosensitivity and severe liver damage in humans due to the accumulation of fluorescent protoporphyrin IX (PPIX). While zebrafish () models for porphyria exist, the utility of ferrochelatase () knockout zebrafish, which exhibit EPP, for therapeutic screening and biological studies remains unexplored. This study investigated the use of clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-mediated -knockout zebrafish larvae as a model of EPP1 for drug screening.

View Article and Find Full Text PDF

Objective: Acute intermittent porphyria (AIP) is a rare metabolic disorder caused by haploinsufficiency of hepatic porphobilinogen deaminase (PBGD), the third enzyme of the heme biosynthesis. Individuals with AIP experience neurovisceral attacks closely associated with hepatic overproduction of potentially neurotoxic heme precursors.

Design: We replicated AIP in non-human primates (NHPs) through selective knockdown of the hepatic gene and evaluated the safety and therapeutic efficacy of human PBGD (hPBGD) mRNA rescue.

View Article and Find Full Text PDF

The toxic effect of oxidized-heme, also known as hemin, is implicated in developing adverse clinical outcome in various hematolytic diseases. To simulate and reconstruct the molecular events associated with hemin exposure on circulating monocytes, we employed a THP-1 cell line based in vitro model. Flow cytometry and Western blot analyses were subsequently applied.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!