Necrosis lymphoid tissue

In all tested organisms, PCBs — especially PCBs with 2,3,7,8-TCDD-like activity — adversely affected patterns of survival, reproduction, growth, metabolism, and accumulation. Common manifestations of PCB exposure in animals include hepatotoxicity (hepatomegaly, necrosis), immunotox-icity (atrophy of lymphoid tissues, suppressed antibody responses), neurotoxicity (impaired behavior and development, catecholamine alterations), increased abortion, low birth weight, embryolethality, teratogenicity, gastrointestinal ulceration and necrosis, bronchitis, dermal toxicity (chloracne, edema,... 

In animals, histological examination of lymphoid organs including the thymus and spleen did not reveal treatment-related lesions at dose levels up to 100 mg/kg/day rats (Harleman and Seinen 1979 Kociba et al. 1971, 1977a). Depletion and necrosis of lymphoid tissue in the lymph nodes, spleen, and thymus were noted in mice exposed to lethal doses of hexachlorobutadiene in the 2-week component of the NTP (1991) study. However no abnormalities in these tissues were seen after 13-week exposures to doses of up to 19.2 mg/kg/day (NTP 1991 Yang et al. 1989). Tests on effects of immune function have not been evaluated. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

When administered by intraperitoneal injection, azaspiracid cattsed similar lesions to those reported for oral administration Besides fatly liver and necrosis of lymphoid tissues, i.p. administration to mice induced netrrologic symptoms that included spasm and paralysis of the limbs (Ito et al. 1998). 

Physical changes in the lung after exposure to aerosolized JP-8 may also underlie the altered systemic effects on lymphoid tissue. Robledo and Witten (1999) reported that treatment of mice with substance P, a neurokinin receptor agonist, protected the lungs from the damaging effects of aerosolized JP-8, including increased permeability, epithelial necrosis, and perivascular edema. Substance P administration was also reported to prevent the loss of spleen and thymus cellularity after JP-8 exposure (250-2,500 mg/m3) and to partially restore the proliferative response of spleen cells to Con A + IL-2 (Harris et al. 1997c). 

In animal studies, when the AZA is administered per os, it caused degeneration of epithelial cells and necrosis of the lamina propria in the villi of the small intestine and in lymphoid tissues such as thymus, spleen, and the Peyer s patches fat accumulation in the liver and degeneration of hepatocytes reduction of nongranulocytes and damage to T- and B-cells in the spleen. Overall, AZAl induced a far greater degree of tissue injury and slower recovery time when compared with OA [62,63]. 

Mouse D. alcalai Wrifiiing soon after injection, diarrhea, paralysis, dyspnea. Deafii between 3 and 5 hr at 1.5 jig/kg. No deafiis at 1.0 jlg/kg at 24 h Peritonitis, ascites, necrosis of lymphocytes in lymphoid tissues. Intestinal congestion and hemorrhage. Edema and necrosis of intestinal villi. Decreased weights of fiiymus, spleen and liver [92]... 

Ultrasonography detects ulceration within the thickened wall in only a few cases, whereas it is seen frequently during small bowel follow through examination or barium enema studies. This low sensitivity for the detection of ulcers on sonography may be due to the associated spasm (Kedar 1994). Lymphoid tissue involvement in the ileal wall with ulceration, necrosis, fibrosis, and often with extensive granulomatous infiltrate can be observed (Khaw 1991). In a few cases of intestinal tuberculosis, a spasm of the cecum is identified by a collapsed lumen and irritability of the thickened wall (Lee et al. 1993). 

TCDD are associated with alterations of cell proliferation in affected tissues. Common examples of 2,3,7,8-TCDD-mediated differentiation and proliferation in both fishes and mammals include dermal hyperkeratinization (fin necrosis in fish), teratogenicity, lymphoid involution, immunotoxicity, and carcinogenesis. Lipid peroxidation in liver, kidney, thymus, and testes is induced in rats by 2,3,7,8-TCDD in a dose- and time-dependent maimer. The enhanced lipid peroxidation by microsomes from 2,3,7,8-TCDD-treated rats may be associated with an increase in hydrogen peroxide production in conjunction with a decrease in glutathione peroxidase activity and an increase in free iron. 

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