Prophylactic Action of Linseed (<i>Linum usitatissimum</i>) Oil Against Cyclophosphamide-Induced Oxidative Stress in Mouse Brain

Bhatia, A.L.; Manda, Kailash; Patni, Shikha; Sharma, Antim Lata

doi:10.1089/jmf.2006.9.261

Cited by 51 publications

(34 citation statements)

References 19 publications

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“…Atm encodes a protein Ser/Thr kinase that helps to maintain genomic stability by activating proteins involved in the G 1 /S and G 2 /M cell-cycle checkpoints in response to DNA damage, telomeric instability, or oxidative stress. 52,53 Studies of Atm Ϫ/Ϫ (ATM KO) mice have implicated this kinase both in the intrinsic maintenance of HSC self-renewal and in the maintenance of appropriate bone mass in vivo 21,22,24 ; however, whether these represent completely independent or linked biologic roles of ATM has not been clear. Thus, in light of the activity of ATM in both blood and bone cells, and in cellular responses to DNA damage and oxidative stress (such as occurs in the context of cell death induced by Cy treatment 52-54 ), we hypothesized that ATM may additionally function in regulating intercellular communication between osteoblasts and HSCs.…”

Section: Atm Mediates the Mobilization-induced Changes In Osteoblastimentioning

confidence: 99%

Osteolineage niche cells initiate hematopoietic stem cell mobilization

Mayack

Wagers

2008

Blood

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Recent studies have implicated bonelining osteoblasts as important regulators of hematopoietic stem cell (HSC) self-renewal and differentiation; however, because much of the evidence supporting this notion derives from indirect in vivo experiments, which are unavoidably complicated by the presence of other cell types within the complex bone marrow milieu, the sufficiency of osteoblasts in modulating HSC activity has remained controversial. To address this, we prospectively isolated mouse osteoblasts, using a novel flow cytometry-based approach, and directly tested their activity as HSC niche cells and their role in cyclophosphamide/granulocyte colony-stimulating factor (G-CSF)-induced HSC proliferation and mobilization. We found that osteoblasts expand rapidly after cyclophosphamide/G-CSF treatment and exhibit phenotypic and functional changes that directly influence HSC proliferation and maintenance of reconstituting potential. Effects of mobilization on osteoblast number and function depend on the function of ataxia telangiectasia mutated (ATM), the product of the Atm gene, demonstrating a new role for ATM in stem cell niche activity. These studies demonstrate that signals from osteoblasts can directly initiate and modulate HSC proliferation in the context of mobilization. This work also establishes that direct interaction with osteolineage niche cells, in the absence of additional environmental inputs, is sufficient to modulate stem cell activity. (Blood. 2008;112:519-531) IntroductionMature blood cells have a finite lifespan that necessitates their constant replenishment from self-renewing, multipotent hematopoietic stem cells (HSCs). 1 HSC maintenance and expansion are thought to be regulated by interactions with bone marrow (BM) stromal elements, including osteoblasts 2-4 and vascular endothelial cells, 5 both of which have been proposed to form a supportive HSC "niche." 2,[6][7][8] Osteoblasts, in particular, have been implicated in controlling HSC numbers, and studies in gene-targeted 2 and hormone-treated 6,9 mice show a strong correlation between experimentally induced expansion of osteoblasts and increased HSC frequency. Significantly, most studies of osteoblast function as it relates to HSC have relied on complex in vivo models [10][11][12][13] or on in vitro systems in which osteoblasts are derived ex vivo by extended culture of calvarial precursor cells. 10 Although clearly suggestive, these in vivo analyses are complicated by the unavoidable presence of other, nonosteoblastic cell types, whereas in vitro studies of culture-derived osteoblasts are challenged by the possibility that extended culture may induce changes in osteoblast behavior and/or may fail to properly recapitulate the in vivo conditions under which osteoblasts normally would be formed or regulated. For these reasons, it has been difficult to establish the particular aspects of HSC function that depend on the osteoblastic niche, and this has generated significant controversy regarding the specific role of osteoblasts in HSC regulatio...

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Section: Atm Mediates the Mobilization-induced Changes In Osteoblastimentioning

confidence: 99%

Osteolineage niche cells initiate hematopoietic stem cell mobilization

Mayack

Wagers

2008

Blood

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“…Acrolein interferes with the tissue antioxidant defense system, produces highly reactive oxygen free radicals and is mutagenic to mammalian cells [32]. It was reported that treatment with CPA caused oxidative stress in different organs including brain [33], liver [34] and kidney [15]. Thus, the nephrotoxicity recorded in the current study may be attributed to oxidative stress induced by CPA.…”

Section: Fig9 Effect Of Different Treatments On Creatininementioning

confidence: 60%

Cyclophosphamide Induced Histologial and Immunohistochemical Alterations in Kidney of Albino Rats: The Ameliorative Effect of Fennel Oil

Sakr¹,

El-messady²

2017

ijSciences

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Cyclophosphamide (CPA) is a nitrogen mustard alkylating agent from the oxazaphosphorine group. It is used as an anticancer, anti-neoplastic agents and immunosuppressive agent widely used in chemotherapy. Fennel oil is traditionally used as a treatment for different diseases. The present work studied the effect of Fennel oil on CPAinduced nephrotoxicity in albino rats. Male albino rats were divided into 4 groups; gp1; control, gp2: Each rat was orally given Fennel oil (1 ml/kg body weight once a week for six weeks), gp3: animals were each orally treated with CPA at a dose of 15mg/kg body weight once a week for six weeks, gp4: CPA plus Fennel oil treated group. The obtained results showed that CPA induced histopathological alterations in the kidney including intertubular leucocytic infiltrations,congestion of blood vessels, degeneration of renal tubules and atrophy of glomeruli. Immunohistochemical observations revealed increase in expression of PCNA, caspase-3 and α -SMA. In addition, creatinine and urea levels increased in sera of treated rats. Treating rats with CPA and fennel oil caused an improvement in the histological structure of the kidney and decreased PCNA, caspase-3 and α-SMA. Moreover, creatinine and urea values were decreased. In conclusion, fennel oil showed ameliorative effect against nephrotoxicity of CPA due to its antioxidant activity.

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“…Dietary supplementation of flaxseed was also found to inhibit the growth and development of prostate cancer in the transgenic adenocarcinoma mouse prostate model (Lin et al, 2002). Our previous studies showed that the cyclophosphamide-induced decline in the blood levels of glutathione (GSH) and glutathione peroxidase (GSH-Px) and alkaline phosphatase was also significantly reduced by flaxseed oil in mice (Bhatia et al, 2006).…”

Section: Introductionmentioning

confidence: 98%

Prophylactic effect of flaxseed oil against radiation‐induced hepatotoxicity in mice

Bhatia

Sharma

Patni

et al. 2007

Phytotherapy Research

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Flaxseed (linseed, Linum usitatissimum, Linaceae) is widely used for its edible oil in many parts of the world. The present study investigates the radioprotective and antioxidative potential of flaxseed oil (FO). Swiss albino mice were administered FO orally once daily for 15 consecutive days, then exposed to a single dose of 5 Gy of gamma radiation. Lipid peroxide, reduced glutathione and total protein were estimated in the liver. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), acid and alkaline phosphatase estimations in serum were also carried out. Radiation-induced increases in the levels of lipid peroxidation (LPO), AST, ALT and acid phosphatase were significantly ameliorated by flaxseed oil pretreatment, and radiation-induced depletion in the level of glutathione (GSH) and alkaline phosphatase activities was significantly inhibited by flaxseed oil administration. The lifespan was increased in the flaxseed oil treated irradiated mice in comparison with their respective control mice, with survival data showing an LD(50/30) (lethal dose for 50% of animals after 30 days) of 7.1 and 10 Gy for control and FO treated irradiated mice, respectively, and produced a dose reduction factor for flaxseed oil (DRF) of 1.40. Radiation-induced deficits in body and organ weight were significantly reduced or prevented in flaxseed oil pretreated mice. The protection afforded by flaxseed oil may be attributed to the constituents of the oil, which include omega-3 essential fatty acids and phytoestrogenic lignans, which appear to play an important role in free radical scavenging and singlet oxygen quenching. The study does not rule out the possibility of a prophylactic potential of flaxseed oil against radiation-induced degenerative changes in liver.

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Prophylactic Action of Linseed (Linum usitatissimum) Oil Against Cyclophosphamide-Induced Oxidative Stress in Mouse Brain

Cited by 51 publications

References 19 publications

Osteolineage niche cells initiate hematopoietic stem cell mobilization

Osteolineage niche cells initiate hematopoietic stem cell mobilization

Cyclophosphamide Induced Histologial and Immunohistochemical Alterations in Kidney of Albino Rats: The Ameliorative Effect of Fennel Oil

Prophylactic effect of flaxseed oil against radiation‐induced hepatotoxicity in mice

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