Circadian periodicity of tissue glutathione and its relationship with lipid peroxidation in rats

Farooqui, Mohammed Y. H.; Ahmed, Ahmed E.

doi:10.1016/0024-3205(84)90430-2

Cited by 80 publications

(24 citation statements)

References 19 publications

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“…Luo et al (1997) have shown that, in clinically healthy volunteers, the plasma SOD and malondialdehyde undergo a significant circadian rhythm, peaking around 21:00 h and 15:00 h, respectively. The antioxidants such as catalase (CAT) and reduced glutathione (GSH) show maximal activity around 08:00 in control and around 04:30 h in constant light (Farooqui & Ahmed 1984) treated animals. The decreased mesor of SOD, catalase and GSH showed that the defense mechanism protects the body by utilising these antioxidants to scavenge of excess free radicals produced (Hardeland et al 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Twenty-four hour rhythms of TBARS (Solar & Ahlers 1997), catalase and GSH (Farooqui & Ahmed 1984), SOD (Hodoglugil et al 1995), glucose (Challet et al 2004), cholesterol synthesis (Jones & Schoeller 1990), total protein (Berezkin et al 1992), and AST (Coll et al 1993) were well documented in many laboratories. We have reported marked circadian variation of these parameters in different animal experiments in our lab Subramanian et al 2005).…”

Section: Introductionmentioning

confidence: 97%

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Constant light influences the circadian oscillations of circulatory lipid peroxidation, antioxidants and some biochemical variables in rats

Subash

Subramanian

Sivaperumal

et al. 2006

Biological Rhythm Research

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Temporal oscillations of circulatory thiobarbituric acid reactive substances (TBARS), antioxidants such as reduced glutathione (GSH), superoxide dismutase (SOD), and catalase and glucose, cholesterol, total protein and aspartate transaminase (AST) were studied under LD (12:12 h) and constant light (LL) (500 lux) conditions after exposing the animal for 21 days. Advances in the acrophase of GSH, SOD, catalase, glucose, total protein and (AST) rhythms and delays in TBARS and cholesterol were found; amplitude and mesor values of these rhythms were found to be altered during constant light treatment. The above said circadian alterations during LL exposure may be due to (1) formation of photooxidants and stress mediated lipid peroxidation, suppression of melatonin (2) modulation of neuroendocrine and neurotransmitters rhythm (3) suppression of sleep -wake cycle (4) feeding and locomotion rhythm. The exact mechanism still remains to be explored and further research needed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Constant light influences the circadian oscillations of circulatory lipid peroxidation, antioxidants and some biochemical variables in rats

Subash

Subramanian

Sivaperumal

et al. 2006

Biological Rhythm Research

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“…Wide ranges in GSH concentrations and turnover rates have been reported for hepatic as well as other tissues. Potentially important factors that may influence the GSH, BU, and BMO kinetics and that were not incorporated in the model include: nonenzymic reactions (Malvoisin and Roberfroid 1982;Kreuzer et al 1991) extrahepatic production, conjugation, and elimination of GSH, diurnal variations (Jaeger et al 1973;Farooqui and Ahmed 1984;Jaeschke andWendel 1985, White et al 1987) and feedback regulation (Lauterburg et al 1980;Lauterburg and Mitchell 1981;Kornbrust and Bus 1984) of GSH kinetics. Glutathione-S-transferase is composed by several subunits and exists as several isozymes, each with a different affinity (Mannervik 1985).…”

Section: Model Constraintsmentioning

confidence: 98%

A physiologically based pharmacokinetic model for butadiene and its metabolite butadiene monoxide in rat and mouse and its significance for risk extrapolation

Johanson

Filser²

1993

Arch Toxicol

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The gas 1,3-butadiene (BU) is an important industrial chemical and an environmental air pollutant. BU has been shown to be a weak carcinogen in the rat but a potent carcinogen in the B6C3F1 mouse. This species difference makes risk extrapolation to humans difficult and the underlying mechanism should be clarified before meaningful risk extrapolation to humans can be made. One possible explanation for the species differences in cancer response is that there are quantitative species differences in the formation of genotoxic epoxides. To investigate this possibility a physiologically based pharmacokinetic (pbpk) model for BU together with its first reactive metabolite 1,2-epoxybutene-3 (butadiene monoxide, BMO) was developed. Previously reported values on hepatic glutathione (GSH) turnover, depletion of hepatic GSH in rodents exposed to BU, and in vitro metabolic data of BU and BMO were included in the model, which incorporates intrahepatic first-pass hydrolysis of BMO and the ordered sequential, ping-pong mechanism to describe the enzyme kinetics of BMO-GSH conjugation. In vitro studies were carried out to obtain tissue: air partition coefficients of BU and BMO in rat tissue homogenates. The simulated pharmacokinetics of BU, BMO, and GSH agreed with previously published experimental observations in rat and mouse obtained in closed and open chamber experiments. According to the model, the internal dose of BMO (expressed either as the concentration in mixed venous blood or as the area under the concentration-time curve) is approximately 1.6 times higher in the mouse than in the rat for exposure to BU below 1000 ppm. At higher exposure levels, GSH depletion occurs in the mouse, but not in the rat, after about 6-9 h. This GSH depletion results in up to 2-3 times higher internal doses in the mouse than in the rat. The clear but relatively small species differences in body burdens of BMO indicated from our model can only partly explain the marked species difference in cancer response between mice and rats exposed to BU.

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“…Of note, this dose was also active in several tumor types in the xenograft tumor model (Table 1). Thiol levels were analyzed in control mice at several time points throughout the day to account for any diurnal fluctuations in thiol levels [17]. Analysis of erythrocytes revealed that imexon treatment led to a transient decrease and subsequent recovery of reduced and oxidized glutathione levels over a 6-h time period after dosing (Fig.…”

Section: Biomarker Analysismentioning

confidence: 99%

Preclinical antitumor activity, pharmacokinetics and pharmacodynamics of imexon in mice

Pourpak¹,

Meyers²,

Samulitis³

et al. 2006

Anti-Cancer Drugs

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Imexon, a novel pro-oxidant, thiol-binding agent, is currently in phase I/II clinical trials in patients with advanced solid tumors. The aim of this study was to characterize the preclinical pharmacology of imexon in vivo. We investigated the anticancer activity of imexon in several cancer cell lines grown as xenografts in severe combined immunodeficient mice. Imexon was active against both hematologic and solid tumor types. The maximally tolerated dose, at the selected dosing schedule, was 150 mg/kg. Using the maximally tolerated dose of imexon, we sought to identify a potential pharmacodynamic biomarker to monitor the mechanistic effect systemically. As imexon binds cellular thiols in vitro, thiol depletion by imexon in vivo was evaluated as a potential biomarker. Following a single 150 mg/kg dose of imexon by intraperitoneal injection, glutathione levels decreased by 40% at 3 h in mouse erythrocytes. In mouse plasma, imexon treatment led to a significant decrease in cystine levels 2-4 h after drug administration. Notably, by this time, free imexon plasma levels were nondetectable. By investigating the pharmacokinetics of imexon, we also found that imexon undergoes rapid clearance from plasma in a dose-independent fashion with a half-life of 12-15 min. In summary, imexon is active against several cancer types in vivo. Imexon also decreases circulating thiols and exhibits dose-independent pharmacokinetics in mice. Plasma cystine levels may represent a biomarker of imexon activity in vivo.

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Circadian periodicity of tissue glutathione and its relationship with lipid peroxidation in rats

Cited by 80 publications

References 19 publications

Constant light influences the circadian oscillations of circulatory lipid peroxidation, antioxidants and some biochemical variables in rats

Constant light influences the circadian oscillations of circulatory lipid peroxidation, antioxidants and some biochemical variables in rats

A physiologically based pharmacokinetic model for butadiene and its metabolite butadiene monoxide in rat and mouse and its significance for risk extrapolation

Preclinical antitumor activity, pharmacokinetics and pharmacodynamics of imexon in mice

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