Abstract

The roles of dietary protein (Pr) and calcium (Ca) levels on the changes in T-lymphocyte subsets induced by excessive fluoride (F) intake were assessed using rats that were malnourished for 120 days as a model. The CD⁴⁺ and CD⁸⁺ T-lymphocytes in the spleen tissue were determined by flow cytometry and immunofluorescence assay. The percentages of CD³⁺ , CD⁴⁺ , and CD⁸⁺ T-lymphocytes were reduced in the spleen of rats exposed to excessive F, and malnutrition aggravated these changes in the T-lymphocytes. In addition, the mRNA expression levels of IL-1B, IL-2, IL-6, TNF-a, and IFN-y in the spleen were downregulated significantly. We also reported herein the increased apoptosis ratio following caspase-9 and caspase-3 upregulation in the spleen of rats exposed to excessive amount of F. Light and transmisison electron microscopy revealed the irregularly arranged lymphocytes, few lymph nodules and the apoptotic characteristic of lymphocytes, which are caused by the increased expression of caspase. In addition, Pr and Ca supplementation reversed the morphologic and T-lymphocytic changes in spleen under malnutrition. Taken together, our results revealed an endogenous caspase-mediated mechanism of regulating the apoptosis of the T-lymphocyte subsets, as well as the immune-related cytokine secretion, which reduces the immune function in F-induced rats.

• Related Studies :

  • Some characteristics of fluoride-induced cell death in rat thymocytes: cytotoxicity of sodium fluoride

    Fluoride is found in the atmosphere, water, soil, coal, food, dental and industrial uses. There were some case reports concerning acute fluoride poisoning in workplaces and laboratories. However, there is limited information concerning the mechanism of fluoride-induced cell death. To study the cytotoxicity of fluoride, the effect of sodium fluoride

  • Effects of dietary protein and calcium on thymus apoptosis induced by fluoride in female rats (Wistar rats)

    Our previous studies showed that excessive fluoride (F) ingestion seriously damaged the nonspecific immune function in rabbits. However, the underlying mechanisms of the F-induced damage to the immune system are unclear. The purpose of this study was to investigate whether F induces thymus apoptosis in female rats and its underlying

  • Effect of dietary protein or calcium supplement on the expression of collagen I and dentine phosphoprotein of rats with dental fluorosis.

    This study aims to assess the roles of dietary protein (Pr) and calcium (Ca) levels associated with excessive fluoride (F) intake and the impact of Pr, Ca, and F on expression of collagen I (COL I) and dentine phosphoprotein (DPP) in rat incisors. Seventy-two rats were randomly allotted to six

  • Effects of malnutrition and supplemented nutrition on nonspecific immune function changes induced by fluoride in rabbits

    This study was designed to investigate the protective role of protein (Pr) and calcium (Ca) on effects of fluoride (F) induced in nonspecific immunological function in New Zealand rabbits fed a Pr and a Ca nutritionally deficient (malnutrition) diet. Eighty healthy 30-day-old rabbits (1.07±0.25 kg) were divided randomly into four equal groups of twenty

  • Arsenic and fluoride co-exposure affects the expression of apoptotic and inflammatory genes and proteins in mononuclear cells from children

    Humans may be exposed to arsenic (As) and fluoride (F) through water consumption. However, the interaction between these two elements and gene expression in apoptosis or inflammatory processes in children has not been thoroughly investigated. Herein, the expression of cIAP-1, XIAP, TNF-?, ENA-78, survivin, CD25, and CD40 was evaluated by

• Related FAN Content :

  • Nutrient Deficiencies Enhance Fluoride Toxicity

    It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,

  • Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease

    Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur

  • Factors which increase the risk for skeletal fluorosis

    The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.

  • Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence

    A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.

  • Fluoridated Water Causes Severe Dental Fluorosis in Children with Diabetes Insipidus

    This section on Diabetes includes: • Fluoride & Impaired Glucose Tolerance • Fluoride & Insulin • Fluoride Sensitivity Among Diabetics • Fluoridated Water Causes Severe Dental Fluorosis in Children with Diabetes Insipidus • NRC (2006): Fluoride’s Effect on Glucose Metabolism Excessive exposure to fluoride causes a defect of the tooth enamel known as dental fluorosis. In