The potential relationship between gasotransmitters and oxidative stress, inflammation and apoptosis in lead-induced hepatotoxicity in rats
| Autor: | Rasha B. Abd-ellatief, Ahmed O. Abdel-Zaher, Noha A. Aboulhagag, Fahmy M.M. AL-Wasei, Hanan S.M. Farghaly |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male Inflammation Sodium hydrosulfide Apoptosis Pharmacology Biology medicine.disease_cause Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Rats Wistar Gasotransmitters Cell Biology General Medicine Rats Heme oxygenase 030104 developmental biology chemistry Lead Nitrosative Stress 030220 oncology & carcinogenesis Heme Oxygenase (Decyclizing) Cytokines Liver function medicine.symptom Chemical and Drug Induced Liver Injury Nitric Oxide Synthase Oxidative stress Developmental Biology |
| Zdroj: | Tissuecell. 71 |
| ISSN: | 1532-3072 |
| Popis: | The interrelationship between gasotransmitters and oxidative stress, inflammation and apoptosis in lead-induced hepatotoxicity was investigated in this study. On prolonged exposure, lead was accumulated in liver tissue of rats and impaired liver function and structure as assessed by measurement of the serum hepatic function markers and by histopathological examination. The accumulated metal induced oxidative stress, inflammation and apoptosis in the liver. Also, it increased nitric oxide (NO) production and decreased hydrogen sulfide (H2S) level and heme oxygenase (HO-1) concentration in liver tissue. Decreasing of NO production by L-N(G)-nitroarginine methyl ester (L-NAME) and increasing of H2S level by sodium hydrosulfide (NaHS) and carbon monoxide (CO) level by carbon monoxide-releasing molecule-A1 (CORM-A1) inhibited lead-induced impairment of liver function and structure. Concomitantly, these agents inhibited lead intoxication-induced oxidative stress, inflammation, apoptosis, nitrosative stress and reduction of HO-1 concentration and H2S level. Furthermore, concurrent treatment with these agents inhibited lead intoxication-induced increase in the protein expressions of inducible NO synthase, tumor necrosis factor-alpha, interleukin-1beta and caspase-3 as well as decrease in protein expressions of HO-1 and cystathionine-γ-lyase in the liver. NO donor, l-arginine and H2S and CO biosynthesis inhibitors, trifluoro-DL-alanine and zinc deutroporphyrin, respectively aggravated the toxic effects of lead. These results indicate, for the first time, that there is an interrelationship between gasotransmitters and lead-induced hepatotoxicity. The ability of L-N AME, NaHS and CORM-A1 to provide protective effects against lead-induced hepatotoxicity may positively correlate, to their ability to suppress hepatic oxidative stress, nitrosative stress, inflammation and apoptosis. |
| Databáze: | OpenAIRE |
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