Inflammation Necrosis

In mice exposure to 9 ppm caused a 50% decrease in respiratory rate. Lesions included ulceration and necrosis of the respiratory epithelium and moderate damage to lung tissue. Rats administered, via oral gavage, 10, 20, 40, or 80mg/kg for 10 consecutive days or 32 mg/kg for 90 consecutive days had inflammation, necrosis, acantholysis, hyperkeratosis, and epithelial hyperplasia of the forestomach. Chloropicrin was genotoxic in bacterial test systems."... 

Toxic or potentially toxic agents may be inhaled into the respiratory tract where they may cause localized effects such as irritation (e.g., ammonia, chlorine gas), inflammation, necrosis, and cancer. Chemicals may also be absorbed by the lungs into the circulatory system, thereby leading to systemic toxicity (e.g., CO, lead). 

Dermal effects observed in animals after direct application of potassium dichromate to their skin include inflammation, necrosis, corrosion, eschar formation, and edema in rabbits (Gad et al. 1986) and skin ulcers in guinea pigs (Samitz 1970 Samitz and Epstein 1962). 

Intranasal use, a common method of cocaine abuse, can damage the sinonasal tract, causing acute and chronic inflammation, necrosis, and osteocartilaginous erosion (SEDA-17, 36). These conditions occur secondary to the combined effects of direct trauma from instrumentation, vasoconstriction of small blood vessels with resultant ischemic necrosis, and chemical irritation from adulterants. Intranasal cocaine users can develop septal perforation, saddle-nose deformities, and sinonasal structural damage. 

Three adolescents taking therapeutic doses of minocycline for 12-20 months met the 1993 International Autoimmune Hepatitis Group criteria for autoimmune hepatitis. All had hypogammaglobulinemia and positive antinuclear antibody and antismooth muscle antibody titers. Two underwent liver biopsy that showed severe chronic lymphoplasmocytic inflammation, necrosis, and fibrosis. All other causes of liver disease were excluded. One patient had resolution of symptoms after withdrawal of the drug, while two required immunosuppressive therapy. 

Following an oral gavage for 90 days, the no-effect-dose is 8 mg kg day, with severe forestomach tissue lesions characterized by inflammation, necrosis, acantholysis, hyperkeratosis, and epithelial hyperplasia. Mice exposed to 8 ppm chloropicrin vapor for 6 h day for 5 days developed moderate to severe degeneration of the respiratory and olfactory epithelium as well as fibrosing peribronchitis and peribronchiolitis of the lung. 

The presence of larvae and cysts of T. spiralis may cause localised inflammation, necrosis, damage of muscle fibres and increased eosinophil counts. Sometimes death may occur due to toxemia, trichinous encephalitis or myocardial damage caused by invasion of musculature by the larvae. 

As new compounds, very limited research has been done to evaluate the biological effects of ionic liquids. The topical effect of [EMIM]C1/A1C13 melts and [EMIMjCl on the integument of laboratory rat has been investigated. The study reports that [EMIMjCl is not in itself responsible for tissue damage. However, the chloroaluminate salt can induce tissue irritation, inflammation, and necrosis, due to the presence of aluminium chloride. However, treatments for aluminium chloride and hydrochloric acid are well documented. This study needs to be expanded to the other ionic liquids, and their toxicity need to be investigated [46]. 

Systemic treatment of 13-cis retinoic acid frequently leads to cheilitis and eye irritations (e.g., unspecific cornea inflammation). Also other symptoms such as headache, pruritus, alopecia, pains of joints and bone, and exostosis formation have been reported. Notably, an increase of very low density lipoproteins and triglycerides accompanied by a decrease of the high density lipoproteins has been reported in 10-20% of treated patients. Transiently, liver function markers can increase during oral retinoid therapy. Etretinate causes the side effects of 13-cis retinoid acid at lower doses. In addition to this, generalized edema and centrilobulary toxic liver cell necrosis have been observed. 

Tumor Necrosis Factor a TNF Receptor Superfamily Cytokines Inflammation... 

Human tumor necrosis factor (TNF) (Fig. 1) is a hormone-like proinflammatory peptide belonging to the group of cytokines. It is mainly produced by cells of the immune system in response to infection, inflammation, or cell damage. Disregulated TNF is an important factor in many pathological situations, like sqDsis, rheumatoid arthritis, inflammatory bowel disease (Crohn s disease), and Cachexia. The cytotoxic activity of TNF is of interest in development of new antitumoral strategies. 

The histopathological features of PM may be radically different from those of JDM and ADM. There is little, if any, evidence of involvement of the micro vasculature and the muscle necrosis which occurs appears to be the direct result of targeting of individual muscle fibers. In the dermatomyositis syndromes, antibody-dependent humoral mechanisms are predominant and B-lymphocytes are seen to be the most abundant cell type in almost all JDM cases and a substantial proportion of ADM cases. In contrast, most muscle biopsies from PM patients show evidence of inflammation in which TS (cytotoxic) lymphocytes predominate (Figure 20). Moreover, the distribution of inflammatory cell infiltrates tends to be different. Instead of the mainly perifascicular location of lymphocytes in JDM/ADM, there... 

M (more severe necrosis inflammation, dilation, and congestion of central veins and sinusoids)... 

Inflammatory cytokines have been implicated in the pathophysiology of HF.9 Several proinflammatory (e.g., tumor necrosis factor-a [TNF-a], interleukin-1, interleukin-6, and interferon-y) and anti-inflammatory cytokines (e.g., interleukin-10) are overexpressed in the failing heart. The most is known about TNF-a, a pleiotrophic cytokine that acts as a negative inotrope, stimulates cardiac cell apoptosis, uncouples 3-adrenergic receptors from adenylyl cyclase, and is related to cardiac cachexia. The exact role of cytokines and inflammation in HF pathophysiology continues to be studied. 

Eosinophils may be increased in some patients, particularly during exacerbations. Activated inflammatory cells release a variety of mediators, most notably leukotriene B4, interleukin-8, and tumor necrosis factor-a (TNF-a). Various proteinases, such as elastase, cathepsin G, and proteinase-3, are secreted by activated neutrophils. These mediators and proteinases are capable of sustaining inflammation and damaging lung structures. 

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