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.
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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
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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
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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
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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
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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
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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,
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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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Fluoride & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
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