High Levels of Oxidative Stress Exist in the Brain than Serum or Kidneys in Stroke-Prone Spontaneously Hypertensive Rats at Ten Weeks of Age

10週齢の正常血圧WKYラットと脳卒中易発性高血圧自然発症ラット(SHRSP)の脳、血清および腎における酸化ストレスを測定した。WKYと比べてSHRSPの血清では酸化ストレスの指標である後期蛋白酸化産物(AOPP)、酸化アルブミンおよび酸化蛋白質の濃度が低かった。免疫ブロット法で定量される酸化蛋白質はSHRSPの脳で増加していたが、腎では増加していなかった。リアルタイムPCRで定量されるSODのmRNAおよび免疫ブロット法で定量されるカタラーゼ蛋白質はSHRSPの脳で増加していた。10週齢SHRSPでは血清や腎よりも脳で酸化ストレスが高いが、その原因はSODおよびカタラーゼの低下ではない。10週齢の正常血圧WKYラットと脳卒中易発性高血圧自然発症ラット(SHRSP)の脳、血清および腎における酸化ストレスを測定した。WKYと比べてSHRSPの血清では酸化ストレスの指標である後期蛋白酸化産物(AOPP)、酸化アルブミンおよび酸化蛋白質の濃度が低かった。免疫ブロット法で定量される酸化蛋白質はSHRSPの脳で増加していたが、腎では増加していなかった。リアルタイムPCRで定量されるSODのmRNAおよび免疫ブロット法で定量されるカタラーゼ蛋白質はSHRSPの脳で増加していた。10週齢SHRSPでは血清や腎よりも脳で酸化ストレスが高いが、その原因はSODおよびカタラーゼの低下ではない

Allergen endotoxins induce T-cell–dependent and non–IgE-mediated nasal hypersensitivity in mice

Background: Allergen-mediated cross-linking of IgE on mast cells/basophils is a well-recognized trigger for type 1 allergic diseases such as allergic rhinitis (AR). However, allergens may not be the sole trigger for AR, and several allergic-like reactions are induced by non–IgE-mediated mechanisms. Objective: We sought to describe a novel non–IgE-mediated, endotoxin-triggered nasal type-1-hypersensitivity-like reaction in mice. Methods: To investigate whether endotoxin affects sneezing responses, mice were intraperitoneally immunized with ovalbumin (OVA), then nasally challenged with endotoxin-free or endotoxin-containing OVA. To investigate the role of T cells and mechanisms of the endotoxin-induced response, mice were adoptively transferred with in vitro–differentiated OVA-specific TH2 cells, then nasally challenged with endotoxin-free or endotoxin-containing OVA. Results: Endotoxin-containing, but not endotoxin-free, OVA elicited sneezing responses in mice independent from IgE-mediated signaling. OVA-specific TH2 cell adoptive transfer to mice demonstrated that local activation of antigen-specific TH2 cells was required for the response. The Toll-like receptor 4-myeloid differentiation factor 88 signaling pathway was indispensable for endotoxin-containing OVA-elicited rhinitis. In addition, LPS directly triggered sneezing responses in OVA-specific TH2-transferred and nasally endotoxin-free OVA–primed mice. Although antihistamines suppressed sneezing responses, mast-cell/basophil-depleted mice had normal sneezing responses to endotoxin-containing OVA. Clodronate treatment abrogated endotoxin-containing OVA-elicited rhinitis, suggesting the involvement of monocytes/macrophages in this response. Conclusions: Antigen-specific nasal activation of CD4+ T cells followed by endotoxin exposure induces mast cell/basophil-independent histamine release in the nose that elicits sneezing responses. Thus, environmental or nasal residential bacteria may exacerbate AR symptoms. In addition, this novel phenomenon might explain currently unknown mechanisms in allergic(-like) disorders

Antioxidant properties of some different molecular weight chitosans

Chitosan, a cationic polysaccharide, is widely employed as dietary supplement and in pharmacological and biomedical applications. Although numerous studies have focused on its applications as pharmaceutical excipients or bioactive reagents, relationships between molecular weight (Mr) and biological properties remain unclear. The focus of this study was on the antioxidant properties of several Mr chitosans. We measured the ability of seven Mr chitosans (CT1; 2.8 kDa, CT2; 17.0 kDa, CT3; 33.5 kDa, CT4; 62.6 kDa, CT5; 87.7 kDa, CT6; 604 kDa, CT7; 931 kDa) to protect plasma protein from oxidation by peroxyl radicals derived from 2,2′-azobis (2-amidinopropane) dihydrochloride (AAPH). A comparison of the antioxidant action of high Mr chitosans (CT6–CT7) with that of low Mr chitosans (CT1–CT5) showed that low Mr chitosans (CT1–CT5) were more effective in preventing the formation of carbonyl groups in plasma protein exposed to peroxyl radicals. AAPH substantially increases plasma protein carbonyl content via the oxidation of human serum albumin (HSA). We also measured the ability of these chitosans to protect HSA against oxidation by AAPH. Low Mr chitosans (CT1–CT5) were found to effectively prevent the formation of carbonyl groups in HSA, when exposed to peroxyl radicals. Low Mr chitosans were also good scavengers of N-centered radicals, but high Mr chitosans were much less effective. We also found a strong correlation between antioxidant activity and the Mr of chitosans in vitro. These activities were also determined by using the ‘TPAC’ test. These results suggest that low Mr chitosans (CT1–CT3) may be absorbed well from the gastrointestinal tract and inhibit neutrophil activation and oxidation of serum albumin that is frequently observed in patients plasma undergoing hemodialysis, resulting in a reduction in oxidative stress associated with uremia.7 page(s