The luminescent land snail Dyakia striata displayed a bioluminescence spectrum with a maximum wavelength of 515 nm. A green fluorescent substance extracted from the photogenic organ of an adult snail had a similar wavelength maximum but its fluorescence spectrum differed from that of flavin chromophore substances involved in light emission in some other luminescent organisms.

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Mouse liver microsomal cholesterol epoxide hydrolase: a specific inhibition of its activity by 5,6 alpha-Imino-5 alpha-cholestan-3 alpha-OL.

A comparative study on mouse liver epoxide hydrolase activities has been done by using enzyme inhibitors in order to obtain evidence for the specificity of microsomal cholesterol epoxide hydrolase. 5,6 alpha-Imino-5 alpha-cholestan-3 beta-ol (IC) strongly inhibited the microsomal hydrolysis of cholesterol alpha-epoxide and the other delta 5-steroid alpha-epoxides (0.1 mM each) at concentrations less than 1 microM but affected neither microsomal nor cytosolic hydrolysis of any other epoxides of endogenous and exogenous compounds (0.1 mM each). On the other hand, 3,3,3-trichloropropene 1,2-oxide (TCPO) did not inhibited the microsomal hydrolysis of delta 5-steroid alpha-epoxides but strongly inhibited both microsomal and cytosolic hydrolysis of the other epoxides used. The only exceptions for the epoxy substrates that were not affected by both inhibitors were 5 alpha-cholest-2-ene alpha- and beta-epoxides. The inhibition by IC of the microsomal cholesterol alpha-epoxide hydrolysis was competitive, but no significant inhibition of the enzyme activity was observed by the typical microsomal xenobiotic substrates, hexadecene oxide and benzo[a]pyrene 4,5-oxide. These results strongly suggest that the microsomal enzyme hydrolyzing cholesterol alpha-epoxide differs from the microsomal hydrolase for epoxides of various xenobiotic olefins and arenes.

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PubMedDate not supplied

A specific COX-2 inhibitor attenuates cell infiltration but does not prolong graft survival in murine cardiac transplantation.

COX-2 is a key factor in the progression of inflammation, the effects of a specific COX-2 inhibitor in cardiac transplantation have not yet been elucidated. To test the hypothesis that a COX-2 inhibitor can alter cardiac rejection, we analyzed graft survival using totally allomismatched grafts. Although the COX-2 inhibitor attenuated myocardial cell infiltration, the inhibitor did not prolong survival. We conclude that the COX-2 inhibition may have potential for the suppression of inflammation in cardiac allografts.

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PubMedDate not supplied

Catechins attenuate myocardial cell infiltration and fibrosis but do not prolong graft survival in murine cardiac allografts.

Although tea catechins have many biological functions, their effects on cardiac allograft rejection have not been well studied. We used a total allomismatch heart transplant model to test the effects of catechins in cardiac rejection. We have shown that cell infiltration and fibrosis were suppressed in catechin-treated allografts compared with nontreated transplants. However, catechins did not statistically prolong graft survival. We conclude that catechins have a potential to suppress inflammation in cardiac allografts.

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PubMedDate not supplied