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Characteristics of persistent organic pollutants (POPs) because of its long-term persistence, bioaccumulation, semi-volatile and highly toxic, and has become one of the most talked about environmental contaminants. Conference of the Parties to the Stockholm Convention in May 2009 decided to add nine chemicals PFOS (Perfluorooctane sulfonate PFOS) and its salts included in the Convention on the controlled range. PFOA (perfluorooctanoic acid, PFOA) has caused widespread concern in society as one of the potential carcinogens. In this paper, the research progress at home and abroad, BALB / c mice as test animals, respectively, with a normal diet (regular diet, RD) and high fat diet (high-fat diet, HFD) feeding, feeding smaller of two feed The mice were exposed to concentrations of 0,5,10,20 mg / kg / d PFOS or PFOA studies PFOS and PFOA exposure caused immune organ atrophy and lipid metabolism, to study the potential cause of the immune system toxic mechanism. The experimental results show that: the after of PFOS exposure 14d, RD exposed body weight of mice were significantly decreased, severe atrophy of the spleen and thymus. The histopathology results show exposed mice, thymic cortex and medulla boundaries are unknown, spleen sinus expansion. Increased apoptosis in the thymus. Meanwhile, PFOS caused thymus peroxisome proliferator-activated receptor a (PPARa) and interleukin (IL-1β) up-regulation of gene expression, but no significant difference. HFD group, these phenomena still exists and has not been eliminated. In addition, PFOA exposure to the same the RD mice weight can cause a significant decline, severe atrophy of the spleen and thymus, and reduce the number of blood lymphocytes. The mouse thymus cortex and medulla boundaries unclear, seen interstitial fiber components hyperplasia in the spleen and thymus can be observed to a large number of cell apoptosis. Spleen superoxide dismutase (SOD) activity and hydrogen peroxide (H202) content did not change significantly. PFOA exposure can cause thymus PPARα, peroxisome proliferator-activated receptor γ (PPARγ) and upregulation of IL-1β gene expression and glucocorticoid receptor (GR). HFD group of PFOA caused toxic effects persists, slightly decreased, but the degree of injury related to the level of gene expression and RD exposure group compared, no significant difference. The results showed that, after exposure to PFOS or PFOA, ultra-microscopic structure of the thymus and spleen cells had similar damage, specific performance cavitation cells mitochondrial swelling and deformity nucleus organization vacuolization transmission electron microscopy (TEM), The large amount of apoptosis and lipofuscin. Primary cultures of thymus cells and spleen cells were exposed to PFOS or PFOA, high concentrations of PFOS and PFOA were able to cause cell death. And in vivo exposure experiment, primary cultured cells apoptosis ratio has not changed significantly change. These results indicate that: PFOS and PFOA can cause aging of the immune organ atrophy of the spleen and thymus lymphocyte apoptosis and recession; the mice extra large intake of fat, and not significantly weaken the immune toxicity of PFOS and PFOA; despite PFOS and PFOA causes immunosuppression by interfering with lipid metabolism, but this is not the only way to cause immune suppression caused by PFOS and PFOA immunotoxicity should be the result of the combined effects of a variety of ways.
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