AI Article Synopsis

  • The study investigated how TCDD, a toxic compound, impacts c-src-deficient mice compared to their wild-type counterparts.
  • N6 src-/+ mice showed significantly less toxicity response to TCDD, including less weight loss and lower liver and pancreas weight changes, compared to N6 src+/+ mice.
  • The results suggest that lacking c-src expression influences the severity of TCDD-induced effects, particularly related to metabolic changes like glycogen depletion and triglyceride accumulation in the liver.

Article Abstract

The effect of TCDD was studied in c-src-deficient C57BL6-src(tm1sor) (N6 src -/- and -/+) mice, and their wild-type littermate mice (N6 src +/+). The former was created from the original strain of B6, 129-src(tm1sor) mice through six generations of backcrossings with C57BL6 mice. The results of a high dose TCDD toxicity tests in male mice indicated that N6 src-/+ mice were significantly less responsive to the toxic action of TCDD (115 microg/kg single i.p. injection) than N6 src+/+ mice in terms of reduced % body weight gain, the increase in the liver to body weight ratio, and the decrease in the adipose tissue to liver weight ratio and in the weight of pancreas. To understand the cause for these differential effects of TCDD we studied TCDD-induced changes in several biochemical parameters at day 10 and found that most drastically affected ones were glycogen depletion and phosphoenolpyruvate carboxykinase (PEPCK) downregulation. In addition, the degree of triglyceride accumulation in liver was less pronounced in N6-/+ than in N6+/+ mice. These findings suggest that the absence of c-src expression indeed affects the development of selected, TCDD-induced toxic endpoints that are related to wasting syndrome.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0300-483x(02)00006-9DOI Listing

Publication Analysis

Top Keywords

mice
10
generations backcrossings
8
tcdd studied
8
body weight
8
weight ratio
8
tcdd
5
effects src-deficiency
4
src-deficiency expression
4
expression vivo
4
vivo toxicity
4

Similar Publications

Diabetic cardiomyopathy (DCM) is a major complication of type 2 diabetes mellitus (T2DM), but its effective prevention and treatment are still limited. We investigated the effects of GYY4137, a slow-releasing hydrogen sulfide donor, and its downstream mediator forkhead box protein O1 (FOXO1) on T2DM-associated DCM. , T2DM mice were induced by a high-fat diet coupled with streptozotocin injection.

View Article and Find Full Text PDF

The anti-tumor effect of the IFNγ/Fas chimera expressed on CT26 tumor cells.

Anim Cells Syst (Seoul)

January 2025

Department of Biochemistry, College of Natural Sciences, Chungnam National University, Daejeon, Korea.

Interferon gamma (IFNγ) is well-known for its ability to stimulate immune cells in response to pathogen infections and cancer. To develop an effective cancer therapeutic vaccine, CT26 colon carcinoma cells were genetically modified to express IFNγ either as a secreted form (sIFNγ) or as a membrane-bound form. For the membrane-bound expression, IFNγ was fused with Fas (mbIFNγ/Fas), incorporating the extracellular cysteine-rich domains, transmembrane, and cytoplasmic domains of Fas.

View Article and Find Full Text PDF

Alterations in Ileal Secretory Cells of The DSS-Induced Colitis Model Mice.

Acta Histochem Cytochem

December 2024

Department of Anatomy, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahatanishi, Kitakyushu, Fukuoka 807-8555, Japan.

Inflammatory bowel disease is triggered by abnormalities in epithelial barrier function and immunological responses, although its pathogenesis is poorly understood. The dextran sodium sulphate (DSS)-induced colitis model has been used to examine inflammation in the colon. Damage to mucosa primality occurs in the large intestine and scarcely in the small intestine.

View Article and Find Full Text PDF

Generation of high avidity T cell receptors (TCRs) reactive to tumor-associated antigens (TAA) is impaired by tolerance mechanisms, which is an obstacle to effective T cell therapies for cancer treatment. NY-ESO-1, a human cancer-testis antigen, represents an attractive target for such therapies due to its broad expression in different cancer types and the restricted expression in normal tissues. Utilizing transgenic mice with a diverse human TCR repertoire, we isolated effective TCRs against NY-ESO-1 restricted to HLA-A*02:01.

View Article and Find Full Text PDF

Background: Chronic graft-versus-host disease (cGVHD) manifests with characteristics of autoimmune disease with organs attacked by pathogenic helper T cells. Recent studies have highlighted the role of T cells in cGVHD pathogenesis. Due to limited understanding of underlying mechanisms, preventing cGVHD after allogenic hematopoietic cell transplantation (HCT) has become a major challenge.

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!