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Biochemical Methods of Studying Hepatotoxicity
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Prasada Rao S. Kodavanti, Harihara M. Mehendale
(14C)-Citrulline-arsenate reagent: Dissolve 1.75 g of l-citrulline and 15.6 g of dibasic sodium arsenate (Na2AsSO4, 7H2O) in distilled water. To this, add 45.45 μCi of (14C-ureido)-l-citrulline, adjust pH to 7.1, and dilute to a final volume of 100 ml with distilled water. This solution contains 50 μmol of (14C)-citrulline (0.004545 μCi/μmol; 10,000 dpm/μmol) in 0.5 ml of 0.5 M arsenate buffer, pH 7.1.
Ellagic Acid Prevents Oxidative Stress, Inflammation, and Histopathological Alterations in Acrylamide-Induced Hepatotoxicity in Wistar Rats
Published in Journal of Dietary Supplements, 2020
Mohammad Yahya Karimi, Iman Fatemi, Heibatullah Kalantari, Mohammad Amin Mombeini, Saeed Mehrzadi, Mehdi Goudarzi
The equilibrium between antioxidants and free radicals protects the body against the harmful effects of free radicals such as ROS. Previous reports have indicated that ACR decreased the capacity of antioxidant enzymes such as CAT, SOD, GPx, and GSH (He et al. 2017; Rizk et al. 2017). In line with these studies, we showed that ACR (20 mg/kg orally [p.o.]) reduced these antioxidant enzymes. We also demonstrated that administration of EA (30 mg/kg p.o.) simultaneously with ACR restores the activity of GPx and the GSH content. Researchers have reported that EA shows its antioxidant effects indirectly by increasing the activity of antioxidant enzymes. In our previous study, we showed that EA enhances the endogenous antioxidant system to protect against methotrexate-induced hepatotoxicity (Mehrzadi et al. 2018c). It was shown that EA has protective effects in sodium arsenate–induced hepatorenal toxicity in rats via increasing the activity of SOD and GPx (Mehrzadi et al. 2018a).
Zinc and selenium modulate barium-induced oxidative stress, cellular injury and membrane-bound ATPase in the cerebellum of adult rats and their offspring during late pregnancy and early postnatal periods
Published in Archives of Physiology and Biochemistry, 2018
Awatef Elwej, Imen Ghorbel, Mariem Chaabane, Nejla Soudani, Hela Mnif, Tahia Boudawara, Najiba Zeghal, Madiha Sefi
The excess generation of ROS and subsequent oxidative stress induced by BaCl2 mediated functional changes such as the degeneration of cholinergic neurons in brain leading to a cholinergic neurotransmission deficit. In fact, BaCl2 treatment caused a significant decrease of AChE activity in the cerebellum of dams and their pups. Our results were in accordance with a previous study of El-Demerdash et al. (2004) who have reported a decrease of AChE activity in the brain of rats submitted to cadmium. The decrease of AChE activity may be explained, according to Najimi et al. (1997) by the fact that metals can bind to the functional groups of the protein, like imidazole, sulfhydryl and carboxyl groups. Once the enzyme is bound to some of these functional groups, its catalytic activity could be compromised, leading to the loss of enzyme function. Moreover, according to Gottiplu et al. (2006), the inhibition of antioxidant enzymes like CAT and GPx by heavy metals accelerates aggregation of free radicals and induced changes in the electrical charge leading to AChE activity inhibition. In our study, therapeutic role of Se and Zn against deleterious effects of Ba showed an improvement in AChE activity after co-administration of Se or Zn to Ba-treated rats. These trace elements probably protected AChE activity via their antioxidant properties. Our hypothesis was in agreement with the previous findings of Ani et al. (2006) and Amal and Mona (2009) showing that Se and Zn may have a crucial role in the improvement of AChE activities in the brain after exposure of rats to lead acetate and sodium arsenate respectively.
Intravenous arsenic trioxide and all-trans retinoic acid as front-line therapy for low-risk acute promyelocytic leukemia
Published in Expert Review of Hematology, 2019
The first pharmacokinetic studies were performed in 8 relapsed APL patients through gas chromatography by measuring the plasma drug levels [15]. After a first plasma peak level of 6.85 µmol/L, the drug was rapidly eliminated, with a half-life elimination time of 0.89 h. The plasma levels of arsenic fluctuated between 0.1 and 0.5 mol. In the same study, possible changes of arsenic after its long-term administration were evaluated. The results showed that the continuous administration did not alter the plasma concentrations of the drug. High amounts of arsenic appeared in the urine in the same day of the infusion accounting for approximately 1–8% of the total daily dose administered. The urinary excretion of arsenic persisted after withdrawal of the drug, but with a decreased amount. Hair and nails contained traces of arsenic, which increased during administration (a peak of 2.5–2.7 µg/g) and declined after withdrawal of the drug. Mass spectrometry identifies several arsenic compounds such as sodium arsenite, sodium arsenate, sodium methylarsonate (MMAs), dimethyl-arsinic acid (DMAs), trimethylarsine oxide (TMAsO), arsenobetaine (AsBe), arsenocholine (AsCho) and tetramethyl-arsonium (TetMAs). DMAs and MMAs were detected in the serum and urine, and their concentrations increased after 2 h from completion of administration [16]. Au et al. [17] studied the arsenic levels in 67 paired cerebrospinal fluid (CSF) and plasma samples from 9 APL patients receiving oral ATO. The median levels in the CSF and plasma were 95.8 nmol/L (range 3.5–318.9 nmol/L) and 498.9 nmol/L (range 36.3–1892.8 nmol/L), respectively, with CSF levels being 17.7% of the plasma levels. The results suggested that arsenic was present in the CNS at therapeutic concentrations [17].