Environ Sci Technol. 2005 Feb 15;39(4):1084-91. Related Articles, Links


Effect of chlorophyllin-chitosan on excretion of dioxins in a healthy man.

Kitamura K, Nagao M, Hayatsu H, Morita M.

National Institute for Environmental Studies, Tsukuba, Ibaraki 305-8506, Japan. kitamura.kimiyoshi@nies.go.jp

We investigated the usefulness of chitosan and chlorophyllin-chitosan (chl-chitosan) administration for reduction of the body burden of environmental dioxins, including polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDDs/ Fs) and coplanar polychlorinated biphenyls (Co-PCBs), by examining the excretion levels in the feces and sebum of a healthy man. The volunteer ate the same three meals every day during the 40-d experiment, which was composed of five phases (I-V) of 8 d each. In phase I (days 1-8), the volunteer was given only the basal diet. In phases II-V, 0.2 g of chitosan, 0.6 g of chitosan, 0.2 g of chl-chitosan, and 0.6 g of chl-chitosan, respectively, were administered immediately after each meal. We measured daily the amount of dioxins occurring in the feces and sebum during the last 5 d of each phase. The total toxicity equivalency (TEQ) of the dioxin in phases I-V were 27, 26, 38, 36, and 67 pg/d in the feces and 20, 19, 16, 16, and 14 pg/d in the sebum, compared with 74 pg/d in the food. The excretion of dioxins in the feces was significantly increased in phases III, IV, and V, being 140% (p < 0.05), 135% (p < 0.05), and 249% (p < 0.01) of the control level (phase I). Although the dioxin in the sebum was slightly decreased in phase V as compared with the control level, the total amount of excreted dioxin in feces and sebum was increased significantly in phase V, being 174% of the control level, which is almost the same level as that in the food. This indicates that chl-chitosan can prevent accumulation of dioxin, at least at the intake level of normal foods.

PMID: 15773481 [PubMed - indexed for MEDLINE]

Inflammatory events are involved in acne lesion initiation.

J Invest Dermatol. 2003 Jul;121(1):20-7.

Jeremy AH, Holland DB, Roberts SG, Thomson KF, Cunliffe WJ.

University of Leeds, and Leeds General Infirmary, Leeds, UK.

The earliest subclinical acne "lesion" is a microcomedone, of which hyperproliferation of the follicular epithelium is a characteristic feature. Inflammatory cells have been observed at the periphery of these "lesions". This study investigated whether inflammatory events occur pre or post hyperproliferative changes. Cellular, vascular, and proliferative markers were examined by immunohistochemical techniques on biopsies of clinically normal follicles from uninvolved skin and early inflamed lesions from acne patients. Control follicles were obtained from non-acne subjects. Follicles from uninvolved skin exhibited no microcomedonal features. Proliferation in the epithelium was comparable to controls and was significantly lower than in inflamed lesions. Numbers of CD3+, CD4+ T cells were elevated in the perifollicular and papillary dermis although levels were not equivalent to those in papules. The number of macrophages was also greatly increased and similar to those in papules. There were no changes in blood vessel numbers or vascular intercellular adhesion molecule 1 expression but E-selectin expression was increased to levels found in papules and vascular adhesion molecule 1 levels were upregulated. Levels of the pro-inflammatory cytokine interleukin-1 were also upregulated perifollicularly. Moreover, aberrant integrin expression was demonstrated in the epidermis around these uninvolved follicles and inflamed lesions whereas the basement membrane was still intact. These results provide novel evidence for vascular endothelial cell activation and involvement of inflammatory responses in the very earliest stages of acne lesion development.

PMID: 12839559 [PubMed - indexed for MEDLINE]

The effects of roasting on the allergenic properties of peanut proteins.

J Allergy Clin Immunol. 2000 Oct;106(4):763-8.

Maleki SJ, Chung SY, Champagne ET, Raufman JP.

USDA-ARS-Southern Regional Research Center, New Orleans, LA 70124, USA.

BACKGROUND: Because of the widespread use of peanut products, peanut allergenicity is a major health concern in the United States. The effect or effects of thermal processing (roasting) on the allergenic properties of peanut proteins have rarely been addressed. OBJECTIVE: We sought to assess the biochemical effects of roasting on the allergenic properties of peanut proteins. METHODS: Competitive inhibition ELISA was used to compare the IgE-binding properties of roasted and raw peanut extracts. A well-characterized in vitro model was used to test whether the Maillard reaction contributes to the allergenic properties of peanut proteins. The allergic properties were measured by using ELISA, digestion by gastric secretions, and stability of the proteins to heat and degradation. RESULTS: Here we report that roasted peanuts from two different sources bound IgE from patients with peanut allergy at approximately 90-fold higher levels than the raw peanuts from the same peanut cultivars. The purified major allergens Ara h 1 and Ara h 2 were subjected to the Maillard reaction in vitro and compared with corresponding unreacted samples for allergenic properties. Ara h 1 and Ara h 2 bound higher levels of IgE and were more resistant to heat and digestion by gastrointestinal enzymes once they had undergone the Maillard reaction. CONCLUSIONS: The data presented here indicate that thermal processing may play an important role in enhancing the allergenic properties of peanuts and that the protein modifications made by the Maillard reaction contribute to this effect.

PMID: 11031348 [PubMed - indexed for MEDLINE]