Protective role of dimethyl diphenyl bicarboxylate (DDB) against erythromycin induced hepatotoxicity in male rats

Abdel-Hameid, Nassr-Allah H.

doi:10.1016/j.tiv.2006.12.006

Cited by 33 publications

(13 citation statements)

References 22 publications

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“…The hepatotoxicity‐related oxidative stress induced by EMC in normal as well as pregnancy was prereported . In some hepatoprotective models, EMC has been used, for the induction of hepatotoxicity . EMC crosses the placenta and secreted in milk .…”

Section: Discussionmentioning

confidence: 99%

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Erythromycin‐induced genotoxicity and hepatotoxicity in mice pups treated during prenatal and postnatal period

Singh

Mondal

et al. 2013

Fundamemntal Clinical Pharma

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The main aim of this study was to investigate the oxidative stress, genotoxicity and cytotoxicity of erythromycin (EMC) in pups of treated dams in gestation as well as the lactation period (LP). The two doses of EMC were compared using intraperitoneal (i.p.) route in two different periods, that is, in gestation period and in the LP. The rationale behind selection of i.p. route is because of the fact that EMC gets degrades in acidic pH of the stomach. The doses of EMC used were clinically equivalent dose (CED; EMC 14.2 mg/kg, i.p.) and a lower dose (EMC 10 mg/kg, i.p.) than CED. EMC toxicities in mice pups were evaluated using various parameters such as micronucleus (MN) test in peripheral blood and bone marrow, malondialdehyde (MDA) assay, glutathione (GSH reduced) assay and histopathological assessment in liver tissue. The CED of EMC led to a significant increase in MDA and decreased in GSH concentration in pups' liver tissue in both gestation and LPs and also to a significant increase in MN frequency in both peripheral blood and bone marrow cells of pups. There were no significant toxicities at a lower dose than CED. There were also some chronic findings with liver histopathological examination at CED. It is thus concluded that EMC accentuates the oxidative stress, cytotoxicity and DNA damage in pups of their postnatal life; hence, EMC should be avoided in the pregnancy and also in the LP.

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Section: Discussionmentioning

confidence: 99%

“…All values were shown in mean AE SEM (n = 6). induction of hepatotoxicity [10,11]. EMC crosses the placenta [37] and secreted in milk [38,39].…”

Section: Discussionmentioning

confidence: 99%

Erythromycin‐induced genotoxicity and hepatotoxicity in mice pups treated during prenatal and postnatal period

Singh

Mondal

et al. 2013

Fundamemntal Clinical Pharma

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“…and CCl 4 following 5 days of oral treatment with saline [15, 16]. The drug groups received CCl 4 following 5 days of oral treatment with MCE L , MCE M , and MCE H , representing 50, 150, or 450 mg kg −1 MCE [17, 18]. Mice were humanely killed 24 h after the administration of CCl 4 and their blood was collected.…”

Section: Methodsmentioning

confidence: 99%

Myrica rubra Extracts Protect the Liver from CCl₄‐Induced Damage

Gao

Wang

et al. 2011

Evidence-Based Complementary and Alternative Medicine

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The relationship between the expression of mitochondrial voltage-dependent anion channels (VDACs) and the protective effects of Myrica rubra Sieb. Et Zucc fruit extract (MCE) against carbon tetrachloride (CCl4)-induced liver damage was investigated. Pretreatment with 50 mg kg−1, 150 mg kg−1 or 450 mg kg−1 MCE significantly blocked the CCl4-induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels in mice (P < .05 or .01 versus CCl4 group). Ultrastructural observations of decreased nuclear condensation, ameliorated mitochondrial fragmentation of the cristae and less lipid deposition by an electron microscope confirmed the hepatoprotection. The mitochondrial membrane potential dropped from −191.94 ± 8.84 mV to −132.06 ± 12.26 mV (P < .01) after the mice had been treated with CCl4. MCE attenuated CCl4-induced mitochondrial membrane potential dissipation in a dose-dependent manner. At a dose of 150 or 450 mg kg−1 of MCE, the mitochondrial membrane potentials were restored (P < .05). Pretreatment with MCE also prevented the elevation of intra-mitochondrial free calcium as observed in the liver of the CCl4-insulted mice (P < .01 versus CCl4 group). In addition, MCE treatment (50–450 mg kg−1) significantly increased both transcription and translation of VDAC inhibited by CCl4. The above data suggest that MCE mitigates the damage to liver mitochondria induced by CCl4, possibly through the regulation of mitochondrial VDAC, one of the most important proteins in the mitochondrial outer membrane.

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“…Bifendate is widely used for the treatment of chronic hepatitis by lowering alanine transminse (ALT) (Pan et al 2006;Guan et al 2005;Abdel-salam et al 2007;Abdel-Hameid et al 2007;Yao 2005;Cui et al 2002). In China, the combined therapy of bifendate with cyclosporine on patients with a renal transplant is supposed to decrease the side-effect of hepatotoxicity caused by cyclosporine.…”

Section: Introductionmentioning

confidence: 99%

Effect of bifendate on the pharmacokinetics of talinolol in healthy subjects

Zeng

et al. 2009

Xenobiotica

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To evaluate the effect of bifendate on the pharmacokinetics of talinolol, 16 unrelated male healthy subjects were selected for this study. After repeated oral administration of placebo or bifendate (three times daily for 14 days), the plasma concentration of talinolol was measured by high-performance liquid chromatography-electrospray mass spectrometry. This study was carried out in a randomized, single-blinded, placebo-controlled, crossover manner. After the treatment of bifendate, the area under the curve (AUC(0-infinity)) was decreased significantly by 11.2% (90% confidence interval (CI), 7.3-12.4%; p = 0.001), and the Cmax value of talinolol was decreased by approximately 9.7% (90% CI, 5.5-11.4%; p = 0.001). The oral clearance of talinolol was increased significantly by 13.1% (90% CI, 8.0-14.4%; p = 0.001). The results suggest that the treatment of bifendate can decrease the plasma concentration of talinolol in healthy subjects.

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Protective role of dimethyl diphenyl bicarboxylate (DDB) against erythromycin induced hepatotoxicity in male rats

Cited by 33 publications

References 22 publications

Erythromycin‐induced genotoxicity and hepatotoxicity in mice pups treated during prenatal and postnatal period

Erythromycin‐induced genotoxicity and hepatotoxicity in mice pups treated during prenatal and postnatal period

Myrica rubra Extracts Protect the Liver from CCl₄‐Induced Damage

Effect of bifendate on the pharmacokinetics of talinolol in healthy subjects

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Protective role of dimethyl diphenyl bicarboxylate (DDB) against erythromycin induced hepatotoxicity in male rats

Cited by 33 publications

References 22 publications

Erythromycin‐induced genotoxicity and hepatotoxicity in mice pups treated during prenatal and postnatal period

Erythromycin‐induced genotoxicity and hepatotoxicity in mice pups treated during prenatal and postnatal period

Myrica rubra Extracts Protect the Liver from CCl4‐Induced Damage

Effect of bifendate on the pharmacokinetics of talinolol in healthy subjects

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Myrica rubra Extracts Protect the Liver from CCl₄‐Induced Damage