Advances in Clinical Chemistry, Vol. 29 by Herbert E. Spiegel (ed.)

By Herbert E. Spiegel (ed.)

The sector of scientific chemistry now encompasses elements of analytical chemistry, biochemistry, medical laboratory technological know-how, toxicology, immunology and molecular biology. This serial offers a extra complete international view of the present and destiny instructions of this increasing self-discipline. This quantity provides topical papers realted regularly to the kidney, melanoma and functions of the polymerase chain response.

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EXPRESSION OF Mn-SOD in Vitro IN RESPONSE TO TNF AND TPA TREATMENTS As described above, TNF or IL-1 specifically induces mRNA for Mn-SOD and this effect is blocked by actinomycin D but not cyclohexamide, indicating that the increase in Mn-SOD mRNA results from an increase in transcription of the 42 NAOYUKI TANIGUCHI Mn-SOD gene (M12,M15,W10). Lipopolysaccharide also induces Mn-SOD mRNA in pulmonary epithelial cells by a similar mechanism (V3). We showed that phorbol 12-myristate 13-acetate (TPA), a potent tumor promoter and protein kinase C activator, also induced Mn-SOD expression only in TNF-resistanf cell lines and presented two hypothetical signal transducing pathways in this gene expression (F10).

52) reported that no significant change was observed in Cu,Zn-SOD activity in persons with and without senile cataracts. Whether age-related changes occur in Cu,ZnSOD in normal rat lens is now under study in our laboratory. 3. 1. 1. Mn-SOD Protein Mn-SOD is localized in the mitochondria1 matrix and is considered to play an important role in the dismutation of 01in tissues, Due to the limited availability of human tissues, we have determined Mn-SOD levels in rat tissues. As shown in Table 2, heart, small intestine, kidney, and liver contain relatively high amounts.

TNF-sensitive cell. bility is that AP-1 is responsible' for this gene expression. Ho et al. (H15) found the consensus sequence for AP-1 enhancer binding protein in the 5'-flanking region of the rat Mn-SOD gene. TPA acts to both activate AP-1 protein and to enhance protooncogene JunIAP-1 expression. However, there would be more than one pathway because TNF could induce Mn-SOD in the cells that were desensitized to TPA by TPA-pretreatment. Thus, at least two pathways participate in Mn-SOD expression.

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