Modulation of tumor necrosis factor α expression in mouse brain after exposure to aluminum in drinking water

Tsunoda, Masashi; Sharma, Raghubir P.

doi:10.1007/s002040050630

Cited by 39 publications

(27 citation statements)

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“…Both in vitro and in vivo evidence demonstrate that aluminum increases both glutamate levels and pro-inflammatory cytokines like TNF-alpha in the brain [149][150][151][152][153][154], thus promoting an encephalitic reaction cascade. Aluminum has been shown to facilitate increases in intracellular calcium and ROS that are induced by other neurotoxicants, such as glutamate and ferrous iron [155].…”

Section: Environmental Factorsmentioning

confidence: 99%

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Seneff¹,

Lauritzen

Davidson³

et al. 2013

Entropy

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This paper makes two claims: (1) autism can be characterized as a chronic lowgrade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether. OPEN ACCESSEntropy 2013, 15 373

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Section: Environmental Factorsmentioning

confidence: 99%

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Seneff¹,

Lauritzen

Davidson³

et al. 2013

Entropy

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“…The cDNA was synthesized from mRNA using a First-Strand cDNA synthesis kit (Amersham Pharmacia Biotech, Piscataway, NJ). RT-PCR was used to analyze the mRNA expression for TNFα and IL-1β in J774.1 cells, and for β-actin (internal control), as described previously (20). The sense and anti-sense primers used were 5'-GTTCTATGGCCCAGACCCTCACA-3' and 5'-TCCCAGGTATATGGGTTCATACC-3' for TNFα (23), 5'-GCAACTGTTCCTGAACTCA-3' and 5'-CTCGGAGCCT-GTAGTGCAG-3' for IL-1β (24), and 5'-ATGGATGAC-GATATCGCT-3' and 5'-ATGAGGTAGTCTGTCAGGT-3' for β-actin.…”

Section: Measurement Of Cell Viability and Mrna Expression For Cytokinesmentioning

confidence: 99%

“…The mRNA expressions of TNFα and IL-1β in macrophages, evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR), have previously been used as indexes of immunotoxicity (20,21). We evaluated the effects of TBT chloride on TNFα and IL-1β mRNA expression in a murine macrophage lineage cell line, J774.1, in vitro.…”

Section: Introductionmentioning

confidence: 99%

Tributyltin (TBT) increases TNFα mRNA expression and induces apoptosis in the murine macrophage cell line in vitro

Nakano

Tsunoda

Konno

2004

Environ Health Prev Med

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Objective: Tributyltin (TBT) compounds have been widely used as antifouling agents for shipbottom paint. The immune system is a target of TBT intoxication. We evaluated the effects of TBT chloride in macrophages, which have critical roles in the immune system, using a murine macrophage lineage cell line, J774.1, in vitro.Methods: We examined tumor necrosis factor α (TNFα), interleukin-1β (IL-1β) and c-jun mRNA expression in J774.1 cells. The effects of TBT on the apoptosis of J774.1 cells were examined by determining the percentage of TUNEL-positive cells and caspase-3 activity.Results: The mean values of the viabilities of J774.1 cells exposed to TBT decreased dose-dependently. The relative mRNA expression of TNFα increased dose-dependently, however, that of IL-1β was not significantly different among the groups. The mean percentage of TUNEL-positive cells increased dose-dependently. Increases in the caspase-3 activities of J774.1 cells were observed in the groups exposed to higher concentrations of TBT. The mean value of relative mRNA expression of c-Jun transcription factor increased dose-dependently.Conclusions: The increases in the percentage of TUNEL-positive cells and in caspase-3 activity suggested that exposure to TBT induces apoptosis of J774.1 cells. The increases in the mRNA expression of TNFα and c-jun by TBT may be related to apoptosis in macrophages.

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“…RNA isolation and semi-quantitative estimation of cytokine expression RNA was isolated from the tissue using the protocol described earlier (Tsunoda and Sharma 1999). First-strand complimentary DNA (cDNA) was synthesized using Superscript II reverse transcriptase enzyme (Life Technologies, Grand Island, NY, USA).…”

Section: Preparation Of Single-cell Lymphocyte Populationsmentioning

confidence: 99%

Oral exposure to inorganic mercury alters T lymphocyte phenotypes and cytokine expression in BALB/c mice

Kim

Johnson

Sharma

2003

Archives of Toxicology

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Mercury is a well-recognized health hazard and an environmental contaminant. Mercury modulates immune responses ranging from immune suppression to autoimmunity but the mechanisms responsible for these effects are still unclear. Male BALB/c mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm mercury in drinking water for 14 days. Body weight was reduced at the highest dose of mercury whereas the relative kidney and spleen weights were significantly increased. The dose range of mercury used did not cause hepatotoxicity as indicated by circulating alanine aminotransferase and aspartate aminotransferase levels. Circulating blood leukocytes were elevated in mice treated with the highest dose of mercury. Mercury ranging from 1.5 to 37.5 ppm dose-dependently decreased CD3(+) T lymphocytes in spleen; both CD4(+) and CD8(+) single-positive lymphocyte populations were decreased. Exposure to 7.5 and 37.5 ppm mercury decreased the CD8(+) T lymphocyte population in the thymus, whereas double-positive CD4(+)/CD8(+) and CD4(+) thymocytes were not altered. Mercury altered the expression of inflammatory cytokines (tumor necrosis factor alpha, interferon gamma, and interleukin-12), c-myc, and major histocompatibility complex II, in various organs. Results indicated that a decrease in T lymphocyte populations in immune organs and altered cytokine gene expression may contribute to the immunotoxic effects of inorganic mercury.

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Modulation of tumor necrosis factor α expression in mouse brain after exposure to aluminum in drinking water

Cited by 39 publications

References 0 publications

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Tributyltin (TBT) increases TNFα mRNA expression and induces apoptosis in the murine macrophage cell line in vitro

Oral exposure to inorganic mercury alters T lymphocyte phenotypes and cytokine expression in BALB/c mice

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