Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis

Miltonprabu, Selvaraj; Nazimabashir,; Manoharan, Vaihundam

doi:10.1016/j.toxrep.2015.11.010

Cited by 39 publications

(30 citation statements)

References 54 publications

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“…Resveratrol inhibited the F-type ATPase by targeting the F1 sector, which is located in the inner membrane of mitochondria and the plasma membrane of normal endothelial cells and in several cancer cell lines (Zheng et al;1999, Dorrie et al;. Resveratrol has been shown to improve mitochondrial function (Miltonprabu et al;.…”

Section: Mitochondrial Pathwaymentioning

confidence: 99%

Resveratrol as MDR reversion molecule in breast cancer: An overview

Alamolhodaei

Tsatsakis

Ramezani

et al. 2017

Food and Chemical Toxicology

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Breast cancer is the most common cause of cancer mortality among women worldwide; therefore, a strategy to defeat breast cancer is an extremely important medical issue. One of the major challenges in this regard is multidrug resistance (MDR). Resveratrol, a well-known phytoestrogen, may be helpful as part of an overall strategy to defeat breast cancer. The mixed agonist and antagonist role of resveratrol for the estrogen receptor makes it a controversial but interesting molecule in cancer therapy, especially in hormone dependent cancers. Several in vitro investigations have suggested that resveratrol can reverse multidrug resistance. However, poor bioavailability of resveratrol is a potential limitation for resveratrol treatment and cancer outcome in vivo. Fortunately, combination therapy with other selected compounds improves resveratrol's bioavailability and/or a delay in its metabolism. This review summaries the available published literature dealing with the effects of resveratrol on multidrug resistance in cancer and more specifically, breast cancer.

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Section: Mitochondrial Pathwaymentioning

confidence: 99%

Resveratrol as MDR reversion molecule in breast cancer: An overview

Alamolhodaei

Tsatsakis

Ramezani

et al. 2017

Food and Chemical Toxicology

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“…Hepatoprotective effect of grape seed proanthocyanidins were also detected against cadmium induced toxicity in rats [29]. Tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I-III, II-III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption were restored at ordinary levels by grape seed proanthocyaninds following cadmium exposure [29]. However, grape juice concentrate did not modulate metalloproteinases (MMPs) 2 and 9 immunoexpression in cadmium-intoxicated rats [30].…”

Section: Livermentioning

confidence: 99%

Are Grapes Able to Mitigate the Noxious Effects Induced by Cadmium Exposure in Different Tissues and/or Organs? A Mini Review

et al. 2018

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Grapes are fruits that grow in clusters and can be crimson, black, dark blue, yellow, green, orange, and pink. Cadmium is a non-essential metal toxic to living organisms and the environment. Recently, health professionals, food scientists, and consumers have paid much attention to grapes for their health-promoting effects. To the best of our knowledge, there are no reviews describing the ability of grapes to mitigate the toxic effects induced by cadmium exposure in different tissues and/or organs. Herein, the aim of this review is to present the effects of grapes following cadmium exposure on the number of papers published in the scientific literature. The results showed that grapes are able to mitigate the harmful activities induced by exposure to cadmium in several tissues and organs. The main actions are closely related to tissue regeneration as a result of the reestablishment of morphology and antioxidant activity. However, further studies are welcomed in order to elucidate new biological pathways regarding the outcomes promoted by grapes in this context, specially related to inflammation, tissue regeneration and cellular death.

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“…For example, celluar reduced glutathione (GSH) depletion mediated Cd‐induced PTEN degradation and subsequent PI3K/Akt activation and then induced inflammation in RAW264.7 cells (Huang et al, ). In another study, Cd (5 mg/kg body weight) caused enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis (Miltonprabu et al, ). Moreover, it has been reported that maternal exposure to Cd led to accumulation in placental tissues and correlated with increased nuclear factor‐kappaB expression, which was sensitive to inflammation and oxidative stress (Ronco et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have reported that acute/subacute Cd exposure led to oxidative stress and endoplasmic reticulum (ER) stress in different organs (Gobe & Crane, 2010;Ji et al, 2011;Ji et al, 2012;Kitamura & Hiramatsu, 2010;Li et al, 2016). It has also been reported that acute Cd exposure can induce inflammation through oxidative stress mechanisms (Dong et al, 1998;Huang et al, 2014;Miltonprabu et al, 2016;Ronco et al, 2011). For example, celluar reduced glutathione (GSH) depletion mediated Cd-induced PTEN degradation and subsequent PI3K/Akt activation and then induced inflammation in RAW264.7 cells (Huang et al, 2014).…”

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confidence: 99%

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Chronic cadmium exposure induced hepatic cellular stress and inflammation in aged female mice

Zhang

Wang

et al. 2018

J of Applied Toxicology

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Previous studies have revealed that acute cadmium (Cd) exposure led to inflammation in different organs through an oxidative stress mechanism. However, whether chronic Cd exposure induces inflammation in liver and the mechanistic link between inflammation and cell stress remains unclear. In the present study, we investigated the effects of chronic Cd exposure on hepatic cellular stress and inflammatory responses. Female CD1 mice were administrated with CdCl2 (10 and 100 mg/L) in drinking water for 57 weeks. Our results showed that the mRNA levels of Inos and the protein content of HO‐1, markers of oxidative stress, were markedly increased in Cd‐treated mice. In addition, the protein level of GRP78, the chaperone of endoplasmic reticulum (ER) stress, was significantly increased in Cd‐treated mice. The expression of the proteins CHOP and peIF2α, two proteins downstream of ER stress, was also upregulated in the Cd‐100 mg/L and Cd‐10 mg/L group, respectively. Moreover, there were increased inflammatory cells existing in liver after Cd administration. Besides, there was a significant elevation in the mRNA level of Mip‐2, Il‐10 and Il‐12 in the Cd‐100 mg/L group. The mRNA level of Tgf‐β was also upregulated in Cd‐treated mice. Moreover, we also found that the number of Ki67‐positive hepatic cells was increased in the Cd‐10 mg/L group. Hence, our results indicated that chronic Cd exposure induced oxidative stress, ER stress, inflammatory responses and proliferation in the liver of aged female mice.

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Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis

Cited by 39 publications

References 54 publications

Resveratrol as MDR reversion molecule in breast cancer: An overview

Resveratrol as MDR reversion molecule in breast cancer: An overview

Are Grapes Able to Mitigate the Noxious Effects Induced by Cadmium Exposure in Different Tissues and/or Organs? A Mini Review

Chronic cadmium exposure induced hepatic cellular stress and inflammation in aged female mice

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