Effect of cysteine, methionine, ascorbic acid and thiamine on arsenic-induced oxidative stress and biochemical alterations in rats

Nandi, Dilip Kumar; Patra, R C; Swarup, D.

doi:10.1016/j.tox.2005.02.013

Cited by 153 publications

(90 citation statements)

References 33 publications

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“…The inhibitory effect of arsenic on protein profile is in agreement with the finding of Nandi et al (2005) who reported that arsenic inhibited glucocorticoid hormones, which play important role in protein synthesis and/or metabolism. Accordingly, the reduction in plasma proteins in animals exposed to environmental pollutants could be attributed to the hepatic changes of protein synthesis and the free amino acid metabolism.…”

Section: Discussionsupporting

confidence: 91%

Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation byPistacia lentiscusoil

Klibet

Boumendjel

Khiari

et al. 2015

Pharmaceutical Biology

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Context: Pistacia lentiscus L. (Anacardiaceae) is an evergreen shrub widely distributed throughout the Mediterranean region. Pistacia lentiscus oil (PLo) was particularly known in North African traditional medicine. Thus, people of these regions have used it externally to treat sore throats, burns and wounds, as well as they employed it internally for respiratory allergies. PLo is rich in essential fatty acids, vitamin E and polyphenols. As a very active site of metabolism, liver is reported to be susceptible to arsenic (As) intoxication.Objective: The present study evaluates the protective effect of PLo against sodium arseniteinduced hepatic dysfunction and oxidative stress in experimental Wistar rats. Materials and methods: Twenty-eight rats were equally divided into four groups; the first served as a control, the remaining groups were respectively treated with PLo (3.3 mL/kg body weight), sodium arsenite (5.55 mg/kg body weight) and a combination of sodium arsenite and PLo. After 21 consecutive days, cellular functions were evaluated by hematological, biochemical and oxidative stress markers. Results: A significant decrease in the levels of red blood cells, haemoglobin (p 0.001), hematocrit (p 0.001), reduced glutathione and metallothionein (p 0.05) associated with a significant increase of malondialdehyde (p 0.001) were noticed in the arsenic-exposed group when compared to the control. The As-treated group also exhibited an increase in hepatic antioxidant enzymes namely superoxide dismutase, glutathione peroxidase (p 0.01) and catalase (p 0.05). However, the co-administration of PLo has relatively reduced arsenic effect. Conclusion: The results showed that arsenic intoxication disturbed the liver pro-oxidant/ antioxidant status. PLo co-administration mitigates arsenic-induced oxidative damage in rat.

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Section: Discussionsupporting

confidence: 91%

Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation byPistacia lentiscusoil

Klibet

Boumendjel

Khiari

et al. 2015

Pharmaceutical Biology

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“…The levels of ROS and RNS are balanced by two lines of cell defense including the enzymatic (as the first line) and nonenzymatic (as the second line) antioxidants providing maximal protection against OTS via ROS clearing and scavenging (88). Preventive and therapeutic features of antioxidants are well-known and they have been known to have a critical role in protecting biological sites from oxidative injuries (89)(90)(91)(92). By now, many kinds of fruits, vegetables, plant food materials, and dietary supplementation have been investigated for their antioxidant capabilities (92)(93)(94).…”

Section: Antioxidantsmentioning

confidence: 99%

Neurological Disorders and Oxidative Toxic Stress: A Role of Metal Nanoparticles

Mazdeh

Rahiminejad

Nili‐Ahmadabadi

et al. 2016

Jundishapur J Nat Pharm Prod

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Context: Oxidative stress is a hallmark of many types of neuropathology disorders and underlying mechanism in several neurodegenerative diseases and brain injuries. The CNS is particularly susceptible to oxidative toxic stress (OTS). Reactive oxygen spices are the basic inflammation and neurotoxicity mediators in ischemia/reperfusion injuries. The purpose of the present review is to provide an overview of some nanoparticles (NPs) in developing OTS conditions and neurological disorders. Evidence Acquisition: Here, a nanotechnology approach is evaluated using NPs in human neuronal protection against OTS. It may be wide therapeutic applications in the case of acute and/or chronic neurodegenerative disorders related to OTS. Results: In the brain of mice treated with nanosize TiO 2 , a significant association was found between the ability to induce the production of ROS and metabolic stress in intracellular environments and inflammatory responses in mice brai. The large surface area of AgNPs may efficiently facilitate the radicals generation including ROS in various organs. The production of ROS may cause DNA damage, cellular apoptosis, and activation of the mitogen activated protein kinase (MAPK) pathways which is responsible for regulating many cellular processes. Prolonged and excessive OTS may contribute to the activation of transcription factors and genes responsible for inflammation responses such as NF-κB and AP-1. Furthermore, OTS may contribute to the onset of neurodegenerative diseases. The ability of CuONPs to generate OTS in vitro studies has been demonstrated; however, information on the neurotoxicity of the CuONPs in vivo is low. Conclusions:The NPs-induced OTS may increase the pro-inflammatory responses. On the other hand, administration of antioxidants such as NAC and vitamin C and E prior to exposure to metal NPs significantly decreases OTS conditions.

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“…In normal healthy body ROS and antioxidants remain in balance, and when this balance is disturbed, oxidative stress occurs [15]. Oxidative stress causes oxidative damage to cellular DNA, lipids and proteins, which contributes to cell death [16][17][18][19][20]. Almost 200 enzymes are inactivated by arsenic toxicity, mostly involved in DNA replication, repair and cellular energy pathways.…”

Section: Introductionmentioning

confidence: 99%

Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay

Mahjabeen¹

2016

J Carcinog Mutagen

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Arsenic is metalloid present in measureable quantity in air, water, and soil through natural and anthropogenic sources. It is neurotoxic, hepatotoxic and genotoxic effects, variety of health problems have been associated to arsenic exposure. This review was designed to investigate the possible association between arsenic exposure and DNA damage in animals and humans using comet assay. Total 28 studies were selected for measuring DNA damage by comet assay. Trend of significance in tail length and tail moment was observed using regression analysis. Due to limited number of studies available the regression analysis was non-significant. Individually each study suggested a significant increase in tail moment and tail length in a dose and time-dependent manner. Overall trend observed in this review is the positive association between arsenic exposure either experimentally or occupationally and DNA damage. This initial effort may provide future guideline for the assessment of DNA fragmentation using comet assay.

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Effect of cysteine, methionine, ascorbic acid and thiamine on arsenic-induced oxidative stress and biochemical alterations in rats

Cited by 153 publications

References 33 publications

Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation byPistacia lentiscusoil

Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation byPistacia lentiscusoil

Neurological Disorders and Oxidative Toxic Stress: A Role of Metal Nanoparticles

Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay

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