DNA methylation in the rat livers induced by low dosage isoniazid treatment

Zhang, Bing; Sun, Shiqun; Shen, Lihong; Zu, Xiangyu; Chen, Yi; Hao, Jinqi; Huang, Xiaolin; Fang, Feng

doi:10.1016/j.etap.2011.07.001

Cited by 31 publications

(20 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Dysregulation of physiological germ cells apoptosis leading to spermatogenesis alteration may be a result of external disturbances such as exposure to certain chemotherapeutic agents (Erkkilä et al, 2002;Aitken and Iuliis, 2007). Our results on DNAfragmentation are fully supported by results of other authors, who have established INH negative effects on liver DNA methylation state (Zhang et al, 2011), inhibition of normal DNA synthesis [ ( F i g . _ 3 ) T D $ F I G ] in spermatogonia of male rabbits treated by INH high dose (Burgin et al, 1979) and INH-induced promotion of apoptosis in HepG2 cells with decrease Bcl-2/Bax ratio, leading to caspase-3 and caspase-9 activation (Bhadauria et al, 2010).…”

Section: Discussionsupporting

confidence: 91%

Induction of CYP2E1 in testes of isoniazid-treated rats as possible cause of testicular disorders

et al. 2015

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 91%

Induction of CYP2E1 in testes of isoniazid-treated rats as possible cause of testicular disorders

et al. 2015

View full text Add to dashboard Cite

“…These pathways include direct inhibition of the binding of transcription factors and DNA binding sites, or indirect transcriptional regulation through changes in chromatin conformation, thereby inhibiting the expression of genes of drug-metabolizing enzymes [28,29,30]. By establishing an ADLI model of rat by low-dose isoniazid induction, our previous studies confirmed that methylation level of the whole genome of liver tissue of rats with ADLI was significantly lower than that of the control group [15,16]. Notably, aberrant methylation was also found in the promoter region of the CYP2E1 gene.…”

Section: Discussionmentioning

confidence: 89%

“…If CpG island methylation occurs in genes encoding drug-metabolizing enzymes, it may lead to decline or loss of detoxification activity against toxic metabolites from anti-TB drugs, causing ADLI. A previous study reported that a standard dose of pyrazinamide induced rat liver injury as well as continuous epigenetic change [14], while in another study, 1/3 human dose of isoniazid was found to cause decreased methylation level of whole genomic DNA in rat liver cells and LINE-1 fragment [15]. Furthermore, low dose of isoniazid has been reported to induce hypermethylation of the CYP2E1 promoter region in rats [16].…”

Section: Introductionmentioning

confidence: 99%

Correlation of CpG Island Methylation of the Cytochrome P450 2E1/2D6 Genes with Liver Injury Induced by Anti-Tuberculosis Drugs: A Nested Case-Control Study

Zhang

Zhu

et al. 2016

IJERPH

Self Cite

View full text Add to dashboard Cite

This study investigated the role of CpG island methylation of the CYP2E1 and CYP2D6 genes in liver injury induced by anti-TB drugs from an epigenetic perspective in a Chinese cohort. A 1:1 matched nested case-control study design was applied. Pulmonary tuberculosis (TB) patients, who underwent standard anti-TB therapy and developed liver injury were defined as cases, while those who did not develop liver injury were defined as control. The two groups were matched in terms of sex, treatment regimen, and age. In 114 pairs of cases, CpG island methylation levels of the CYP2E1 and CYP2D6 genes in plasma cell-free DNA were found to be significantly correlated with the occurrence of anti-TB drug-induced liver injury (ADLI), with odds ratio (OR) values of 2.429 and 3.500, respectively (p < 0.01). Moreover, through multivariate logistic regression analysis, CpG island methylation of the CYP2E1 and CYP2D6 genes in plasma cell-free DNA were found to be significantly correlated with the occurrence of ADLI, with adjusted OR values of 4.390 (95% confidence interval (CI): 1.982–9.724) and 9.193 (95% CI: 3.624–25.888), respectively (p < 0.001). These results suggest that aberrantly elevated methylation of CpG islands of the CYP2E1 and CYP2D6 genes in plasma cell-free DNA may increase the risk of ADLI in Chinese TB patients.

show abstract

“…The mechanism of hepatotoxicity effect of TB drugs has been linked to their generation of reactive oxygen species (ROS) [6]. Therefore, hepatic toxicity and hepatitis are common features of rifampicin medication and this has been reported to caused steatosis and increased apoptosis of the hepatocytes and hepatic oxidative stress [7]. Though there is no suitable drug to weaken the hepatotoxicity effect of TB drugs presently [8], herbs are believed to possess potential hepatoprotective agents [9].…”

Section: Introductionmentioning

confidence: 99%

Investigation of Hepatoprotective and Antioxidant Activity of Celosia argentea against Tissue Injury Caused by Rifampicin Administration

Owoade

Adetutu

Olorunnisola

et al. 2019

JALSI

View full text Add to dashboard Cite

This study evaluated the antioxidant and possible protective effects of Celosia argentea against tissue injury caused by rifampicin administration. The antioxidant property of the aqueous extract of C. argentea was assessed in-vitro using 2,2-Diphenyl-1- picrylhydrazyl (DPPH), and 2,2-azino-bis (3-ethylbenzthiazoline-6-sufonic acid) (ABTS) assays. The results obtained revealed the free radical scavenging ability of the extract against the radicals in a concentration-dependent manner. Administration of rifampicin to rats for 28 days induced a significant increase in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and increase cholesterol levels in the plasma, liver and kidney while HDL cholesterol was decreased. It also elevated the levels of malondialdehyde (MDA) and decreased superoxide dismutase (SOD) activities in the liver and kidney. However, co-administration of C. argentea extract to rifampicin treated rats significantly reversed all these rifampicin induced changes. The levels of AST, ALT, ALP and cholesterol in the plasma, liver and kidney were decreased while HDL cholesterol level was increased. In addition, SOD activity was elevated while MDA was depressed when compared to the rifampicin treated rats. The extract of C. argentea was found to be rich in phenolic content and was proved to have no toxic effects on rats when administered alone to normal rats at a dose level of 400mg/kg/day. This study demonstrated that C. argentea leaf extract ameliorates rifampicin-induced hepatotoxicity and could be exploited in the management of hepatotoxic effect associated with rifampicin treatment.

show abstract

DNA methylation in the rat livers induced by low dosage isoniazid treatment

Cited by 31 publications

References 18 publications

Induction of CYP2E1 in testes of isoniazid-treated rats as possible cause of testicular disorders

Induction of CYP2E1 in testes of isoniazid-treated rats as possible cause of testicular disorders

Correlation of CpG Island Methylation of the Cytochrome P450 2E1/2D6 Genes with Liver Injury Induced by Anti-Tuberculosis Drugs: A Nested Case-Control Study

Investigation of Hepatoprotective and Antioxidant Activity of Celosia argentea against Tissue Injury Caused by Rifampicin Administration

Contact Info

Product

Resources

About