intestinal Hg, food hypersensitivity, intestinal-cell damage

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Among thousands of human kids, some would have weak alleles of

glutathione transferase genes, and Watzl et al did not study the

intestinal ramifications of vaccinal ethylmercury secreted into

bile and then into intestinal tract by infants. Watzl et al

conclude that mercury within the gi-tract increases likelihood of

food hypersensitivity.

Food Chem Toxicol 1999 Jun;37(6):627-37

Enhancement of ovalbumin-induced antibody production and mucosal

mast cell

response by mercury.

Watzl B, Abrahamse SL, Treptow-van Lishaut S, Neudecker C, Hansch

GM, Rechkemmer

G, Pool-Zobel BL.

Institute of Nutritional Physiology, Federal Research Centre for

Nutrition,

Karlsruhe, Germany.

Food contaminants may contribute to the recent increased

incidence of food

allergies. We have investigated this hypothesis experimentally.

It was our

objective to determine whether toxicity to the intestinal tissue

by orally

applied mercury (Hg) could modulate the immune response to food

allergens.

Effective mechanisms were studied with functional immunological

and

toxicological parameters. Brown Norway rats were immunized

intraperitoneally by

ovalbumin (OVA). Before oral challenge with OVA, immunized and

non-immunized

animals were exposed to HgCl2. Immunological responses were

measured by

enzyme-linked immunosorbent assays [anti-OVA-IgE and-IgG, rat

mast cell protease

II (RMCPII), interferon-gamma, interleukin-4, lymphocyte

proliferation] and by

flow cytometry (lymphocyte subpopulations). Toxicity of Hg to the

intestinal

barrier was determined by measuring viability, DNA damage and

induction of

glutathione S-transferase in isolated intestinal epithelial cells

and lymph node

cells, and by measuring permeability, short-circuit current and

tissue

conductance of the intact intestinal epithelium. A single high

oral dose of

HgCl2 enhanced the serum concentrations of anti-OVA-IgE and IgG

(P < 0.05) and

of RMCPII (P < 0.05) in immunized rats. The treatment resulted in

a higher

number of CD4/CD25+ T cells in the lymph nodes (P < 0.05). The

multiple

application of low HgCl2 doses (5 x 0.2 mg/kg body weight) only

resulted in an

elevated RMCPII serum concentration (P < 0.05). Neither treatment

schedules

impaired proliferation and cytokine production of lymphocytes. In

non-immunized

rats only minor immunological changes were observed. Oral HgCl2

induced

genotoxic damage in lymph node cells and in jejunal epithelial

cells (P < 0.05).

Moreover, HgCl2 increased the permeability of intestinal

epithelial tissue and

of Caco-2 monolayers and was genotoxic and cytotoxic to isolated

intestinal

epithelial cells in vitro. In conclusion, these studies indicate

that the food

contaminant Hg can stimulate the immune response to OVA in

immunized rats. One

possible mechanism could be the toxicity of Hg to the intestinal

epithelial and

the lymph node cells. Whether humans with allergies respond to

high oral doses

of Hg in a similar way needs to be investigated in further

studies.