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Among the heavy metal poisonings, lead is considered as a major toxic metal causing hematological, neurological, immunological, hepatic, and renal dysfunctions. Lead causes inhibition of ALAD leading to the ALA accumulation inside the cells. Lead also leads to disruption of the anti‐oxidative enzyme system, organ function, and lipid membranes of the cell causing oxidative stress. Zingerone, a phenolic alkanone, is an active edible ingredient present in the ginger that possess varied pharmacological properties. The aim of our study was to evaluate the protective effect of zingerone in lead‐induced toxicity in wistar rats. ALAD concentration was improved in kidney and liver tissues treated with zingerone. Protective effect of zingerone was observed in terms of significant improvement in kidney and liver histology, anti‐oxidant enzyme activity (CAT, SOD, GPx, and GR), organ function parameters, lipid profile, and decreased level of LPO. Therefore, zingerone pretreatment can be a promising agent for alleviation of lead‐induced oxidative damage in cells. Practical applications: Published reports have revealed that consumption of certain bioactive nutrients for example, flavonoids, mineral elements, and vitamins can offer defense from the environmental lead contamination. Zingerone is a strong anti‐oxidant, with very less side effects and has exceptional property of scavenging free radicals, hence reducing the oxidative stresses. This fundamental property of zingerone can alone help in countering the heavy metal toxicity. Different groups have published reported numerous properties of zingerone but as per our understanding till date no study about alleviation of lead toxicity by zingerone in animal model has been undertaken. Hence, we conducted this research to explore the preventive effect of zingerone in lead induced kidney and liver toxicity. The outcome of our study shows potent anti‐oxidant effect and ALAD modulatory property of zingerone which makes it suitable edible candidate for use in countering lead toxicity. [ABSTRACT FROM AUTHOR]

Abstract: This study was designed to assess the potential antifibrotic effect of D‐Limonene—a component of volatile oils extracted from citrus plants. D‐limonene is reported to have numerous therapeutic properties. CCl4‐intduced model of liver fibrosis in Wistar rats is most widely used model to study chemopreventive studies. CCl4‐intoxication significantly increased serum aminotransferases and total cholesterol these effects were prevented by cotreatment with D‐Limonene. Also, CCl4‐intoxication caused depletion of glutathione and other antioxidant enzymes while D‐Limonene preserved them within normal values. Hydroxyproline and malondialdehyde content was increased markedly by CCl4 treatment while D‐Limonene prevented these alterations. Levels of TNF‐α, TGF‐β, and α‐SMA were also assessed; CCl4 increased the expression of α‐SMA, NF‐κB and other downstream inflammatory cascade while D‐Limonene co‐treatment inhibited them. Collectively these findings indicate that D‐Limonene possesses potent antifibrotic effect which may be attributed to its antioxidant and anti‐inflammatory properties. [ABSTRACT FROM AUTHOR]

Background: Epilepsy is a disorder of the central nervous system characterized by recurrent seizures. It is a very common disease in which approximately 30% of patients do not respond favourably to treatment with anticonvulsants. Oxidative stress is associated with neuronal damage arising from epileptic seizures. The present study investigated the effects of naringenin in pilocarpine-induced epilepsy in mice. Naringenin, one of the most frequently occurring flavanone in citrus fruits, was evaluated for its shielding effect against the pilocarpine induced behavioural, oxidative and histopathological alterations in rodent model of epilepsy. Methodology: Epilepsy was induced by giving pilocarpine (300mg/kg) and sodium valproate (300mg/kg) was given as standard anti-epileptic drug Pilocarpine was administered (300 mg /kg body weight) intraperitoneally to the mice on 15th day while naringenin was administered orally (20 and 40 mg/kg body weight) for 15 days prior to administration of pilocarpine. Results: The intraperitoneal administration of pilocarpine enhanced lipid peroxidation, caused reduction in antioxidant enzymes, viz., catalase, superoxide dismutase and glutathione reductase. Treatment of mice orally with naringenin (20 mg/kg body weight and 40 mg/kg body weight) resulted in a significant decrease in lipid peroxidation. There was significant recovery of glutathione content and all the antioxidant enzymes studied. Also in case of behavioural parameters studied, naringenin showed decrease in seizure severity. All these changes were supported by histological observations, which revealed excellent improvement in neuronal damage. Conclusion: The higher dose of naringenin was more potent in our study and was comparable to the standard drug (sodium valproate) in effectiveness. [ABSTRACT FROM AUTHOR]

This study was designed to assess the potential antifibrotic effect of D-Limonene-a component of volatile oils extracted from citrus plants. D-limonene is reported to have numerous therapeutic properties. CCl 4 -intduced model of liver fibrosis in Wistar rats is most widely used model to study chemopreventive studies. CCl 4 -intoxication significantly increased serum aminotransferases and total cholesterol these effects were prevented by cotreatment with D-Limonene. Also, CCl 4 -intoxication caused depletion of glutathione and other antioxidant enzymes while D-Limonene preserved them within normal values. Hydroxyproline and malondialdehyde content was increased markedly by CCl 4 treatment while D-Limonene prevented these alterations. Levels of TNF-α, TGF-β, and α-SMA were also assessed; CCl 4 increased the expression of α-SMA, NF-κB and other downstream inflammatory cascade while D-Limonene co-treatment inhibited them. Collectively these findings indicate that D-Limonene possesses potent antifibrotic effect which may be attributed to its antioxidant and anti-inflammatory properties., (© 2017 Wiley Periodicals, Inc.)

Background: Epilepsy is a disorder of the central nervous system characterized by recurrent seizures. It is a very common disease in which approximately 30% of patients do not respond favourably to treatment with anticonvulsants. Oxidative stress is associated with neuronal damage arising from epileptic seizures. The present study investigated the effects of naringenin in pilocarpine-induced epilepsy in mice. Naringenin, one of the most frequently occurring flavanone in citrus fruits, was evaluated for its shielding effect against the pilocarpine induced behavioural, oxidative and histopathological alterations in rodent model of epilepsy., Methodology: Epilepsy was induced by giving pilocarpine (300mg/kg) and sodium valproate (300mg/kg) was given as standard anti-epileptic drug Pilocarpine was administered (300 mg /kg body weight) intraperitoneally to the mice on 15th day while naringenin was administered orally (20 and 40 mg/kg body weight) for 15 days prior to administration of pilocarpine., Results: The intraperitoneal administration of pilocarpine enhanced lipid peroxidation, caused reduction in antioxidant enzymes, viz., catalase, superoxide dismutase and glutathione reductase. Treatment of mice orally with naringenin (20 mg/kg body weight and 40 mg/kg body weight) resulted in a significant decrease in lipid peroxidation. There was significant recovery of glutathione content and all the antioxidant enzymes studied. Also in case of behavioural parameters studied, naringenin showed decrease in seizure severity. All these changes were supported by histological observations, which revealed excellent improvement in neuronal damage., Conclusion: The higher dose of naringenin was more potent in our study and was comparable to the standard drug (sodium valproate) in effectiveness., Summary: Naringenin ameliorated the development of ROS formation in hippocamus.Naringenin helped in recovery of antioxidant enzymes.Naringenin decreased seizure severity.Naringenin treatment reduced lipid peroxidation. Abbreviations used: 6-OHDA: 6-hydroxydopamine, AED: Anti epileptic drugs, AIDS: Acquired immune deficiency syndrome, ANOVA: Analysis of variance, ATP: Adenosine triphosphate, CA: Cornu ammonis, CAT: Catalase, DG: Dentate gyrus, EDTA: Ethylenediamine tetra acetic acid, GR: Glutathione reductase, GSH: Glutathione reduced, HCl: Hydrochloric acid, IL-1β: Interleukin 1 beta, LPO: Lipid peroxidation, MDA: Malondialdehyde, NADPH: Nicotinamide adenine dinucleotide phosphate, PMS: post mitochondrial supernatant, SE: Status epilepticus, SEM: Standard error of the mean, SOD Superoxide dismutase, TBA: Thiobarbituric acid, TBARS: Thiobarbituric acid reactive substance, TLE: Temporal lobe epilepsy, TNF-α: Tumor necrosis factor alpha., Competing Interests: There are no conflicts of interest.