Paracetamol hepatotoxicity and microsomal function

Kaushal, Ritu; Dave, Kunjan R.; Katyare, Surendra S.

doi:10.1016/s1382-6689(98)00053-2

Cited by 35 publications

(24 citation statements)

References 29 publications

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“…Total protein was estimated using commercially obtained kits from Autospan diagnostics (Bangalore, India), according to the manufacturer's protocol. Plasma ceruloplasmin (Sunderman and Nomoto 1970) and total sulfhydryl groups were also measured (Kaushal et al 1999).…”

Section: Anti-oxidant Statusmentioning

confidence: 99%

Assessment of hepatoprotective and nephroprotective potential of withaferin A on bromobenzene-induced injury in Swiss albino mice: possible involvement of mitochondrial dysfunction and inflammation

Vedi

Sabina

2016

Cell Biol Toxicol

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Bromobenzene is a well-known environmental toxin which causes liver and kidney damage through CYP450-mediated bio-activation to generate reactive metabolites and, consequently, oxidative stress. The present study aimed to evaluate the possible protective role of withaferin A against bromobenzene-induced liver and kidney damage in mice. Withaferin A (10 mg/kg) was administered orally to the mice for 8 days before intragastric intubation of bromobenzene (10 mmol/kg). As results of this experiment, the levels of liver and kidney functional markers, lipid peroxidation, and cytokines (TNF-α and IL-1β) presented an increase and there was a decrease in anti-oxidant activity in the bromobenzene-treated group of mice. Pre-treatment with withaferin A not only significantly decreased the levels of liver and kidney functional markers and cytokines but also reduced oxidative stress, as evidenced by improved anti-oxidant status. In addition, the mitochondrial dysfunction shown through the decrease in the activities of mitochondrial enzymes and imbalance in the Bax/Bcl-2 expression in the livers and kidneys of bromobenzene-treated mice was effectively prevented by pre-administration of withaferin A. These results validated our conviction that bromobenzene caused liver and kidney damage via mitochondrial pathway and withaferin A provided significant protection against it. Thus, withaferin A may have possible usage in clinical liver and kidney diseases in which oxidative stress and mitochondrial dysfunction may be existent.

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Section: Anti-oxidant Statusmentioning

confidence: 99%

Assessment of hepatoprotective and nephroprotective potential of withaferin A on bromobenzene-induced injury in Swiss albino mice: possible involvement of mitochondrial dysfunction and inflammation

Vedi

Sabina

2016

Cell Biol Toxicol

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“…Finally, the mitochondria were suspended in the isolation medium to give about 12-15 mg mitochondrial protein/ml (29,32,38). The post-mitochondrial supernatant was then centrifuged at 12,000 x g for 10 min to remove light mitochondria (39). The pellet was discarded and the resulting supernatant was used as the source of cytosolic enzymes.…”

Section: Animalsmentioning

confidence: 99%

“…Determination of glucose-6-phosphate dehydrogenase (G6PDH) activity (n mole NADPH formed/min/mg protein) was according to the procedure described by Cohen and Rosemeyer (45). Content of glutathione (GSH) (p mole/mg protein) was quantified by the method of Kaushal et al (39).…”

Section: Ros Parametersmentioning

confidence: 99%

Diabetic cardiomyopathy and reactive oxygen species (ROS) related parameters in male and female rats: A comparative study

Akhileshwar

Patel

Katyare

2007

Indian J Clin Biochem

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“…Then the mitochondrial and postmitochondrial fractions were prepared [17] . Lipid peroxides reacts with TBA (thiobarbituric acid) and forms TBARS (thiobarbituric acid reacting substances) giving a characteristic pink color which can be measured colorimetrically at 532 nm indicating the levels of LPO [4] .…”

Section: Antioxidant Parametersmentioning

confidence: 99%

Assessment of Anti-Diabetic Activity of Syzygium jambolanum Using In vitro Model

Bhatt¹,

Barua²,

Gupta³

2009

American J. of Infectious Diseases

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Problem statement: Poor glycemic control and oxidative stress is implicated as a common pathway in the development of diabetic neuropathy. Approach: In the present study, we investigated the protective effects of Enicostemma littorale Blume (EL) (2.5 g kg −1 ), a hypoglycemic and antioxidant herbal medicine in alloxan-induced diabetic neuropathy in male Charles foster rats.Results: Tail flick latency in hot immersion test and the formalin test were used to evaluate nociceptive responses in diabetic rats compared to non-diabetic rats. Preventive treatment of EL (for 45 days) and standard drug glibenclamide (Glib) significantly improved nociception in diabetic rats. The changes in lipid peroxidation status and anti-oxidant enzymes (super-oxide dismutase, glutathione peroxidase and catalase) levels observed in diabetic rats, were significantly restored by EL and glib treatment. Decrease in Na-K + ATPase activity was also significantly restored by EL. Glibenclamide was used as standard drug in present study. Conclusion: This study provided experimental evidence to preventive effect of EL on nerve function and oxidative stress in animal model of diabetic neuropathy. Hence EL may be tried clinically for the treatment of diabetic neuropathy since it was used as folk medicine in diabetic patients.

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Paracetamol hepatotoxicity and microsomal function

Cited by 35 publications

References 29 publications

Assessment of hepatoprotective and nephroprotective potential of withaferin A on bromobenzene-induced injury in Swiss albino mice: possible involvement of mitochondrial dysfunction and inflammation

Assessment of hepatoprotective and nephroprotective potential of withaferin A on bromobenzene-induced injury in Swiss albino mice: possible involvement of mitochondrial dysfunction and inflammation

Diabetic cardiomyopathy and reactive oxygen species (ROS) related parameters in male and female rats: A comparative study

Assessment of Anti-Diabetic Activity of Syzygium jambolanum Using In vitro Model

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