Over-gene expression in the apoptotic, oxidative damage and liver injure in female rats exposed to butralin

Refaie, Amel A.; Ramadan, Amal; Sabry, Nevien M.; Khalil, Wagdy K. B.; Mossa, Abdel‐Tawab H.

doi:10.1007/s11356-020-09416-6

Cited by 15 publications

(13 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All of these parameters are deeply associated with the health of the host animal. For example, a higher content of LDL-C is related to the incidence and severity of cardiovascular disease [14], and elevated liver ALT, AST, and ALP levels are considered hallmarks of liver damage [36]. Our results showed that the HFHCD negatively altered serum lipid metabolism and liver function in the tested mice but did not increase body weight and body fat, which was consistent with a similar study [31].…”

Section: Discussionsupporting

confidence: 92%

A high-fat diet and high-fat and high-cholesterol diet may affect glucose and lipid metabolism differentially through gut microbiota in mice

et al. 2021

View full text Add to dashboard Cite

This study was conducted to investigate the effects of a high-fat diet (HFD) and high-fat and high-cholesterol diet (HFHCD) on glucose and lipid metabolism and on the intestinal microbiota of the host animal. A total of 30 four-week-old female C57BL/6 mice were randomly divided into three groups (n = 10) and fed with a normal diet (ND), HFD, or HFHCD for 12 weeks, respectively. The HFD significantly increased body weight and visceral adipose accumulation and partly lowered oral glucose tolerance compared with the ND and HFHCD. The HFHCD increased liver weight, liver fat infiltration, liver triglycerides, and liver total cholesterol compared with the ND and HFD. Moreover, it increased serum high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total cholesterol compared with the ND and HFD and upregulated alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase significantly. The HFHCD also significantly decreased the α-diversity of the fecal bacteria of the mice, to a greater extent than the HFD. The composition of fecal bacteria among the three groups was apparently different. Compared with the HFHCD-fed mice, the HFD-fed mice had more Oscillospira, Odoribacter, Bacteroides, and [Prevotella], but less [Ruminococcus] and Akkermansia. Cecal short-chain fatty acids were significantly decreased after the mice were fed the HFD or HFHCD for 12 weeks. Our findings indicate that an HFD and HFHCD can alter the glucose and lipid metabolism of the host animal differentially; modifications of intestinal microbiota and their metabolites may be an important underlying mechanism.

show abstract

Section: Discussionsupporting

confidence: 92%

A high-fat diet and high-fat and high-cholesterol diet may affect glucose and lipid metabolism differentially through gut microbiota in mice

et al. 2021

View full text Add to dashboard Cite

show abstract

“…ALP and LDH are widely present in important organs in the human body, and LDH levels increase significantly after liver injury. The combination of ALT, AST, LDH and ALP testing can thus help to improve the diagnostic value for liver injury 29,30 . In our experiment, serum ALT, AST, ALP and LDH levels in mice were significantly increased after CTD exposure and decreased by APS.…”

Section: Discussionmentioning

confidence: 55%

Protective mechanism of Astragalus Polysaccharides against Cantharidin‐induced liver injury determined in vivo by liquid chromatography/mass spectrometry metabolomics

Huang

Tang

Chang

et al. 2021

Basic Clin Pharma Tox

View full text Add to dashboard Cite

Cantharidin (CTD) is a promising anticancer drug; however, its dosage is limited by hepatotoxicity. We previously showed that Astragalus polysaccharides (APS) effectively improved chemical liver injury. In this study, we established a CTD‐induced subacute liver injury mouse model and examined the effects of APS on weight, liver indexes, histopathology, serum biochemical indexes and liver metabolism. Compared with the control group, mice in the CTD model group had obvious liver damage, which was partially prevented by APS. Metabolomics demonstrated that CTD caused liver damage mainly by regulating glycerophospholipid metabolism, ABC transporter pathways and choline metabolism in cancer in vivo. APS regulated primary bile acid biosynthesis and glycerophospholipid metabolism, thus decreasing the liver damage caused by CTD. This study revealed the protective mechanism of APS against CTD‐induced liver injury from the perspective of metabolomics. The results provide an important basis for analysing the mechanism of CTD‐induced liver toxicity and for assessing clinical treatment options to reduce CTD liver toxicity.

show abstract

“…Female rats exposed to butralin increased signi cantly the rate of DNA damage compared with that in control rats. Our previous wok indicated that the ROS formation was raised signi cantly with the exposure to butralin in a dose-dependent manner [27]. It can be suggest that butralin motivated oxidative stress inducing DNA damage by generation of ROS in exposed rats.…”

Section: Discussionmentioning

confidence: 95%

“…Female rats were partitioned into four groups as follows: Group 1, animals were gotten water and lled in as control group; Group 2, rats got Arabic gum at concentration 4.3 g/kg b.wt for 30 days [25]; Group 3, animals got Arabic gum plus butralin (312 mg/L) [27] in drinking water for 30 days. ; Group 4: rats got butralin (312 mg/L) alone in drinking water related to the Acceptable Daily Intake (ADI, 0.5 mg/kg) for rats [28].…”

Section: Animals and Experimental Setupmentioning

confidence: 99%

DNA Damage and Expression Profile of Genes Associated with Nephrotoxicity Induced by Butralin and Ameliorating Effect of Arabic Gum in Female Rats

Refaie

Shalby

Kassem

et al. 2021

Appl Biochem Biotechnol

Self Cite

View full text Add to dashboard Cite

Nephrotoxicity induced by exposure to environmental pollution including herbicides is became global problem. Natural products are the prime alternative of scienti c research as they express better medicinal activity and minor side effects compared with variety of synthetic drugs. This study was performed to evaluate the nephroprotective pro ciency of Arabic gum against butralin-induced nephrotoxicity. Adult female rats were supplemented with Arabic gum (4.3 g/kg b.wt) and/or butralin (312 mg/L) in drinking water for 30 days. The results found that markers of serum kidney function, oxidative stress biomarkers, DNA damage and expression of kidney speci c genes (Acsm2, ACE and ACE2) as well as histopathological examination in treated rats were conducted. Butralin-treated rats showed a rise in serum creatinine, BUN and MDA as well as decrease in activity of the antioxidant markers. In addition, butralin treatment increased the DNA damage, altered the expression levels of Acsm2, ACE and ACE2 and elevated histopathological lesions in kidney tissues. Pretreatment of Arabic gum prevented butralin-prompted degenerative changes of kidney tissues. The results suggested that the protective effect provided by Arabic gum on renal tissues exposed to the herbicide butralin could be attributed to enhancement of antioxidants and increase the free radicals scavenging activity in vivo.

show abstract

Over-gene expression in the apoptotic, oxidative damage and liver injure in female rats exposed to butralin

Cited by 15 publications

References 30 publications

A high-fat diet and high-fat and high-cholesterol diet may affect glucose and lipid metabolism differentially through gut microbiota in mice

A high-fat diet and high-fat and high-cholesterol diet may affect glucose and lipid metabolism differentially through gut microbiota in mice

Protective mechanism of Astragalus Polysaccharides against Cantharidin‐induced liver injury determined in vivo by liquid chromatography/mass spectrometry metabolomics

DNA Damage and Expression Profile of Genes Associated with Nephrotoxicity Induced by Butralin and Ameliorating Effect of Arabic Gum in Female Rats

Contact Info

Product

Resources

About