Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats

Adeyemi, Oluyomi Stephen; Meyakno, Ekong; Akanji, Musbau Adewumi

doi:10.4149/gpb_2016041

Cited by 10 publications

(9 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on the important role of infiltration of neutrophils and monocytes in inflammatory response, we analyzed hepatic and renal MPO activities which have been used as a reliable marker of tissue inflammation. The significant increase in MPO activities of the liver and kidneys tissue after arsenic exposure in our study is consistent with other studies [ 27 ]. We also tested the ALT and AST activities in the serum, which are the important indicators for liver damage and immune response.…”

Section: Discussionsupporting

confidence: 93%

Arsenic Induces Continuous Inflammation and Regulates Th1/Th2/Th17/Treg Balance in Liver and Kidney In Vivo

Duan

et al. 2022

Mediators of Inflammation

View full text Add to dashboard Cite

Numerous studies on arsenic-induced hepatonephric toxicity including cancer have been reported. Given that chronic inflammatory response and immune imbalance are associated with oncogenesis, we investigated whether arsenic could influence the hepatic and nephritic expression of inflammatory factors and the differentiation of T cells. Mice were exposed to NaAsO2 (0, 25, and 50 mg/L) for 1 and 3 months. Our data showed the destruction of the structure and inflammatory infiltration in the liver. The arsenic markedly increased the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The myeloperoxidase (MPO) activities increased in the liver at 25 and 50 mg/L arsenic for 3 months as well as in the kidney at both 1 and 3 months. An increased expression of inflammatory indicators (IL-1β, IL-12, and TNF-α) at 25 and 50 mg/L arsenic for 1 and 3 months in the liver and kidney, as well as IL-1β in the liver for 3 months and in the kidney at 50 mg/L for 1 and 3 months were demonstrated in our experiments. Besides, a definite tendency toward Th1/Th17 cytokines in the liver while Th2/Th17 cytokines in kidney was also observed by arsenic. Moreover, arsenic enhanced the expression of MAPK/Nrf2/NF-κB signaling molecules. In conclusion, the results of the study suggested that arsenic induces continuous immune-inflammatory responses in the liver and kidney.

show abstract

Section: Discussionsupporting

confidence: 93%

Arsenic Induces Continuous Inflammation and Regulates Th1/Th2/Th17/Treg Balance in Liver and Kidney In Vivo

Duan

et al. 2022

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…MPO is present in the cell and all three subtypes of MPO can form a strong complex with DNA to prevent damage during oxidation and ensure the normal differentiation of cell functions [ 36 ]. The increase in MPO content caused by arsenic poisoning may also contribute to lipid peroxidation and oxidative cell damage [ 37 ]. In this study, MPO activity of male rats was greater than that of female rats, which is similar to the results of another study [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Gender difference in arsenic biotransformation is an important metabolic basis for arsenic toxicity

Muhetaer

Yang

Xia

et al. 2022

BMC Pharmacol Toxicol

View full text Add to dashboard Cite

Background Arsenic metabolism enzymes can affect the toxic effects of arsenic. However, the effects of different genders on the metabolites and metabolic enzymes in liver arsenic metabolism is still unclear. This study analyzed the gender differences of various arsenic metabolites and metabolic enzymes and further explored the effects of gender differences on arsenic metabolism in liver tissues of rats. Methods Rats were treated with high/medium/low doses of iAs3+ or iAs5+. Liver pathological changes were observed with electron microscopy. The monomethyl aracid (MMA) and dimethyl aracid (DMA) was determined by high performance liquid chromatography-hydride generation atomic fluorescence spectroscopy. S-adenosylmethionine (SAM), arsenate respiratory reductase (ARR), nicotinamide adenine dinucleotide (NAD), purine nucleoside phosphorylase (PNP), pyruvate kinase (PK), and myeloperoxidase (MPO) SAM, ARR, NAD, PNP, PK, and MPO were determined by enzyme-linked immunoassay. RT-qPCR was used to determine Arsenic (+ 3 oxidation state) methyltransferase (AS3MT). Results The iAs3+ and iAs5+ at high doses induced pathological changes in the liver, such as increased heterochromatin and lipid droplets. Compared within the same group, MMA and DMA were statistically significant in iAs3 + high, iAs3 + medium and iAs5+ low dose groups (P < 0.05). MMA of male rats in iAs3+ high and medium groups was higher than that of female rats, and the DMA of male rats was lower than that of female rats. As3MT mRNA in the male iAs3+ high group was higher than that of females. Besides, compared between male and female, only in iAS3+ low dose, iAS3+ medium dose, iAS5+ low dose, and iAS5+ medium dose groups, there was significant difference in SAM level (P < 0.05). Compared within the same group, male rats had significantly higher PNP and ARR activities while lower PK activity than female rats (P < 0.05). Between the male and female groups, only the iAS3+ high dose and medium dose group had a statistically significant difference (P < 0.05). The NAD activity of females in iAS3+ high dose group was higher than that of males. Conclusion The gender differences in the arsenic metabolism enzymes may affect the biotransformation of arsenic, which may be one of the important mechanisms of arsenic toxicity of different sexes and different target organs.

show abstract

“…MPO is present in the cell and all three subtypes of MPO can form a strong complex with DNA to prevent damage during oxidation and ensure the normal differentiation of cell functions [26]. The increase in MPO content caused by arsenic poisoning may also contribute to lipid peroxidation and oxidative cell damage [27]. In this study, MPO activity of male rats was greater than that of female rats.…”

Section: Discussionmentioning

confidence: 64%

Gender difference in arsenic biotransformation is an important metabolic basis for arsenic toxicity

Muhetaer

Yang

Xia

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: There are gender differences in the biotransformation of arsenic. We investigated the effects of gender differences on arsenic metabolism and arsenic toxicity mechanisms in rat liver tissues. Methods: Rats were treated with different amounts of arsenic compounds. Arsenic form MMA and DMA in the liver was determined by high performance liquid chromatography-hydride generation atomic fluorescence spectroscopy. SAM, ARR, NAD, PNP, PK, and MPO in rat liver were determined by enzyme-linked immunoassay. RT-qPCR was used to determine AS3MT in the liver. Results: Compared with male and female animals in the same group, MMA and DMA were statistically significant in the three groups of iAs3 + high, iAs3 + medium and iAs5+ low (P <0.05). The MMA of male rats in iAs3+ high and medium groups was higher than that of female rats, and the DMA of male rats was lower than that of female rats. As3MT mRNA in the male iAs3+ high group was higher than that of females. Besides, compared between male and female, only in iAS3+ low dose, iAS3+ medium dose, iAS5+ low dose, and iAS5+ medium dose groups, there was significant difference in SAM level (P<0.05). Compared with male and female animals in the same group, male rats had significantly higher PNP and ARR activities while lower PK activity than female rats (P<0.05). Between the male and female groups, only the iAS3+ high dose and medium dose group had a statistically significant difference (P<0.05). The NAD activity of females in iAS3+ high dose group was higher than that of males. Conclusion: Conclusively, under the same arsenic exposure, there were gender differences between female and male rats, and arsenic metabolism was more cytotoxic to male rats than to females.

show abstract

Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats

Cited by 10 publications

References 33 publications

Arsenic Induces Continuous Inflammation and Regulates Th1/Th2/Th17/Treg Balance in Liver and Kidney In Vivo

Arsenic Induces Continuous Inflammation and Regulates Th1/Th2/Th17/Treg Balance in Liver and Kidney In Vivo

Gender difference in arsenic biotransformation is an important metabolic basis for arsenic toxicity

Gender difference in arsenic biotransformation is an important metabolic basis for arsenic toxicity

Contact Info

Product

Resources

About