In this study, the systemic hemodynamics induced by acute and chronic cadmium (Cd+2) intoxication in the cardiovascular system of rats using thoracic electrical bioimpedance were examined and the acute and chronic effects of Cd+2 intoxication on the activities of antioxidant enzymes and malondialdehyde (MDA) were compared. Also, in this study, ultrastructural changes in the heart and aorta of rats were evaluated. Thirty-eight male Wistar albino rats were randomly divided into control, acute, and chronic groups. Chronic group was administered by oral gavage an aqueous solution of CdCl2 for 60 days, at dose of 15 mg Cd+2/kg/day. Acute group was administered by oral gavage an aqueous solution of CdCl2 with a single dose of 15 mg Cd+2/kg. Cadmium increased the stroke volume and cardiac output of rats in the chronic group, but did not change the heart rate significantly. Antioxidant enzymes activities and MDA level significantly increased in the chronic group. In ultrastructural examination, there were widespread degenerative changes in heart muscle cells of the chronic group but endothelial cells and smooth muscle cells in the aorta tissue samples had normal morphological features in all groups. All of the findings indicate that Cd+2 toxication can cause deformation in heart muscle cells due to an increase in free radicals and lipid peroxidation. Also, this study has confirmed that a long-term-Cd+2 exposure increased stroke volume (SV) and cardiac output (CO), but did not change the heart rate (HR).

Download full-text PDF

Source
http://dx.doi.org/10.1080/15376510802662751DOI Listing

Publication Analysis

Top Keywords

acute chronic
16
chronic group
16
muscle cells
12
chronic
8
chronic effects
8
cardiovascular system
8
system rats
8
cd+2 intoxication
8
antioxidant enzymes
8
changes heart
8

Similar Publications

Predictive value of system immune-inflammation index for the severity of coronary stenosis in patients with coronary heart disease and diabetes mellitus.

Sci Rep

December 2024

Department of Endocrinology, The First Clinical Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.

Coronary heart disease (CHD) has been recognized as a chronic progressive inflammatory disorder, and Diabetes mellitus (DM) is an independent risk factor for the pathogenesis of CHD. Recent research has underscored the systemic immune-inflammation index (SII) as a potent prognostic indicator for individuals suffering from acute coronary syndrome (ACS). This study aimed to delve into the relationship between SII and the degree of coronary atherosclerotic stenosis in non-acute myocardial infarction patients with or without DM.

View Article and Find Full Text PDF

Interleukin-6 (IL-6) is a major pro-inflammatory cytokine that demonstrates a robust correlation with age and body mass index (BMI) as part of the senescence-associated secretory phenotype. IL-6 cytokines also play a crucial role in metabolic homeostasis and regenerative processes primarily via the canonical STAT3 pathway. Thus, selective modulation of IL-6 signaling may offer a unique opportunity for therapeutic interventions.

View Article and Find Full Text PDF

Updates on the Pathogenesis of Canine Atopic Dermatitis and Feline Atopic Skin Syndrome: Part 2, the Skin Barrier, the Microbiome, and Immune System Dysfunction.

Vet Clin North Am Small Anim Pract

December 2024

College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 408 Raymond Stotzer Parkway, College Station, TX 77845, USA. Electronic address:

Alterations in the lipid layer and intercellular corneocyte connections can lead to increased allergen penetration through the skin surface. A normal cutaneous microbiome keeps the opportunistic pathogen Staphylococcus pseudintermedius levels low, but allergic inflammation leads to decreased diversity and increase in S pseudintermedius. Keratinocytes sound the initial allergen alarm via cytokine signaling and promote T-helper 2 (Th-2) inflammation.

View Article and Find Full Text PDF

Pharmacological blockade of infection chronification modulates oxy-inflammation and prevents the activation of stress-induced premature senescence markers in schistosomiasis.

Microb Pathog

December 2024

Departamento de Biologia Animal (DBA), Programa de Pós-Graduação em Biologia Animal (PPGBA), Universidade Federal de Viçosa (UFV), Viçosa, 36570-900, Minas Gerais, Brazil.

Chronic inflammation, oxidative stress, and DNA damage are observed in schistosomiasis and premature aging. However, the potential of these events to trigger stress-induced premature senescence (SIPS) throughout schistosomiasis progression remains overlooked, especially in response to the first-line pharmacological treatment. Thus, we investigated the relationship between oxidative stress and SIPS sentinel markers in untreated Schistosoma mansoni-infected mice and those receiving praziquantel (Pz)-based reference treatment.

View Article and Find Full Text PDF

Background: A comprehensive understanding of the molecular pathogenesis of chronic pancreatitis (CP), a fibroinflammatory disorder of the pancreas, is warranted for the development of targeted therapies. The current study focused on comparing the transcriptomes of pancreatic tissues obtained from patients with CP with those of two rodent models of chemically induced CP to identify dysregulated genes/signaling pathways.

Methods: Pancreatitis was induced in mice using cerulein and L-arginine.

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!