beta-alanyl-l-histidine, an anti-oxidant, anti-fibrotic and geno/cytotoxicity inhibitor: a sheild against cc14-induced hepatotoxicity in rats

Hepatic fibrosis is a consequence of chronic liver injury and is characterized by an excessive hepatic connective tissue formation and deposition. p-alanyl-L-histidine [carnosine] is a dipeptide with anti-inflammatory and antioxidant properties in addition to its involvement in many physiological process. Specific treatments to stop progressive liver fibrosis are not available, so that the objective of the present study was to evaluate the hepatoprotective, antioxidant, antifibrotic, cyto/genoprotective effect of p-alanyl-L-histidine against hepatic injury induced by carbon tetrachloride [CCU] in rats. p-alanyl-L-histidine showed significant protection with normalization of liver aminotransferases, increased glutathione S transferase [GST] activity while decreased hepatic hydroxyproline, protein carbonyl, hydrogen peroxide[H[2]O[2]] levels, DNA damage, Cytochrome P450[2]Ei [CYP[2]Ei] activity and transforming growth factor-pi [TGF-pl] mRNA level. In conclusion: P-alanyl-L-histidine possesses hepatoprotective properties through reducing hepatic toxicity markers, oxidative stress, cytotoxicity, genotoxicity, fibrosis and improvement of the histological architecture of the liver

CCl[4] ilnduced hepatotoxicity: protective effects of carnosine on peroxisome proliferator-activated receptor gamma gene expression, genotoxicity and oxidant/antioxidant status in rats

Effect of carnosine as an antioxidant in protection against carbon tetrachloride CCI[4] induced oxidative stress and hepatotoxicity in rats was investigated. Liver toxicity was induced in rat model at which four experimental groups of 20 rats each were constructed: group [1] the control group in which rats were not administrated CCI[4] or carnosine; group [II] CCI[4] group in which rats were subcutaneously injected with CCI[4] in a dose of 2 ml /Kg body weight twice weekly for 4 weeks; group[III] CCI[4] and carnosine group in which rats were also subcutaneously injected with CCI[4] and co-treated with daily intraperitoneal [i.p.] carnosine at a dose of 10 mg / kg body weight and group [IV] received also i.p. repeated daily dose of carnosine. Hepatotoxicity was assessed by measurement of serum aspartate aminotransferase [AST] and alanine aminotransferase [ALT] activities. Hepatic peroxisome proliferator-activated receptor gamma [PPARgammay] mRNA expression, glutathione-S-transferase [GST] activity, paraoxonase 1 [PON1] activity, xantheine oxidase [XO] activity and total anti-oxidant capacity [TAC] level as well as DNA damage in blood were evaluated. The results were confirmed by histopathological examination. Carnosine treatment significantly prevented the CCI[4] induced hepatotoxicity, oxidative stress and DNA damage. In conclusion, our results suggested that carnosine might be a therapeutic antifibrotic/antigenotoxic agent for the treatment of CCI[4-] induced hepatotoxicity due to its antioxidant properties

IgE and histamine levels in tears and serum in relation to clinical types and severity of vernal keratoconjunctivitis

The concentration of IgE antibodies and histamine in tears and serum of [44] patients with vernel keratoconjunctivitis [V.K.C] were measured. The levels compared to the levels in [15] Patients with allergic conjunctivitis [A.C] and [15] normal non atopic controls. It was found that IgE and histamine levels were significantly increased in patients with V.K.C than in patients with A.C, and in both than in normal subjects. IgE and histamine in tears were higher in palpebral than in bulbar V.K.C., and in severe than in mild grades of activity of V.K.C. IgE and histamine in serum were not changed in relation to the types or severity of the disease. After treatment it was obvious that, drop of histamine in tears was rapid and associated with comfort from symptoms, while the decrease in IgE was delayed and was associated with regressim of papillae or corneal infiltration. Accordingly, cortisone was found superior to sodium cromoglycate in management of the severe grade, and both were good in the modrate grade, while antistine privine was of value in the mild grade. One may suggest that determination of tear IgE and histamine are reliable diagnostic tests for management of V.K.C