Modulation of cyclophosphamide-induced early lung injury by curcumin, an anti-inflammatory antioxidant

Venkatesan, Narayanan; Chandrakasan, Gowri

doi:10.1007/bf00928916

Cited by 86 publications

(53 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This observation is in line with many reports that demonstrated apparent elevation in lung TBARS following administration of CP (Patel, 1987;Venkatesan & Chandrakasan, 1995;Stankiewicz et al, 2002). Increased TBARS level observed following CP administration in the current work could be indirectly attributed to the decreased level of GSH; also CP has been proved to induce significant alterations in the activity of NADH and NADPH2, likely to be responsible for the ultrastructural changes within mitochondria which include features of mitochondrial damage with disruption of mitochondrial membranes.…”

Section: Discussionsupporting

confidence: 92%

“…CP metabolism produces highly reactive electrophiles that lead to electrophilic burden on the cells and also due to the formation of acrolein, which deplete GSH contents (McDiarmid et al, 1991). This is in line with other reports that demonstrated GSH reduction or depletion following CP injection in animals (Patel & Block, 1985;Venkatesan & Chandrakasan, 1995;Sulkowska et al, 2002;Manda & Bhatia, 2003). Administration of allicin with CP showed a significant increase in the level of GSH compared to the CP-treated group because it has antioxidant activity (Banerjee et al, 2002).…”

Section: Discussionsupporting

confidence: 78%

See 1 more Smart Citation

Modulation of cyclophosphamide-induced early lung injury by allicin

Ashry

Gameil

Suddеk

2013

Pharmaceutical Biology

View full text Add to dashboard Cite

Context: Cyclophosphamide (CP) causes lung injury in rats through its ability to generate free radicals with subsequent epithelial and endothelial cell damage. Objective: This study was conducted to assess whether allicin can ameliorate CP-induced early lung injury in rats. Materials and methods: Male Sprague Dawely rats were divided into four groups. Group I was the control group. Group II received allicin (50 mg/kg/d, p.o.) for 14 consecutive days. Group III was injected once with CP (150 mg/kg, i.p.). Group IV received allicin for seven consecutive days, before and after CP injection (150 mg/kg, i.p.). The parameters of study were serum biomarkers, lung tissue antioxidant profile and histopathological changes in lung tissue. Results: A single intraperitoneal injection of CP markedly altered the levels of several biomarkers in lung homogenates. Significant increases in lung content of lipid hydroperoxides were seen that paralleled the decreased levels of total reduced glutathione. Superoxide dismutase activity (SOD) was significantly increased. CP increased the level of serum biomarkers; total protein, lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-a). Pretreatment of rats daily with oral allicin seven days prior to and seven days after CP inject significantly inhibited the development of lung injury, prevented the alterations in lung and serum biomarkers associated with inflammatory reactions, with less lipid peroxidation (LP) and restoration of antioxidants. Moreover, allicin attenuated the secretion of proinflammatory cytokine, TNF-a expression in rat serum. In addition, allicin effectively blunted CP-induced histopathological changes in lung tissue. Discussion and conclusion: Our results suggest that allicin is efficient in blunting CP-induced pulmonary damage.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 78%

Modulation of cyclophosphamide-induced early lung injury by allicin

Ashry

Gameil

Suddеk

2013

Pharmaceutical Biology

View full text Add to dashboard Cite

show abstract

“…There is evidence that these agents, particularly cyclophosphamide, result in lipid peroxidation and generation of ROS. The mechanism by which cyclophosphamide kills tumour cell through ROS is demonstrated by rodent data showing that the lung injury associated with treatment with cyclophosphamide is attributable to its ability to generate free radicals (Patel, 1990;Venkatesan and Chandrakasan, 1995). The GSTT1 and GSTM1 enzymes have been shown to have removal activity toward lipid hydroperoxides.…”

Section: Discussionmentioning

confidence: 99%

Glutathione S-transferases (GSTT1 and GSTM1) gene deletions in Tunisians: susceptibility and prognostic implications in breast carcinoma

et al. 2003

View full text Add to dashboard Cite

Glutathione S-transferase Theta1 and Mu1 (GSTT1 and GSTM1) are involved in the metabolism and detoxification of a wide range of potential environmental carcinogens. Conversely, they contribute to tumour cell survival by detoxification of numerous products induced by cancer therapy. The authors designed a large study to investigate the susceptibility and prognostic implications of the GSTT1 and GSTM1 gene deletions in breast carcinoma. The authors used the polymerase chain reaction to characterise the variation of the GSTT1 and GSTM1 genes in 309 unrelated Tunisian patients with breast carcinoma and 242 healthy control subjects. Associations of the clinic-pathologic parameters and the genetic markers with the rates of the breast carcinoma specific overall survival (OVS) and the disease-free survival (DFS) were assessed using univariate and multivariate analyses. A significant association was found between gene deletion of GSTT1 and the risk of early onset of breast carcinoma (OR ¼ 1.60, P ¼ 0.02). The lack of GSTT1 gene deletion was significantly associated with poor clinical response to chemotherapy (OR ¼ 2.29, P ¼ 0.03). This association was significantly higher in patients with axillary's lymph node-negative breast carcinoma (OR ¼ 12.60, P ¼ 0.005). The null-GSTT1 genotype showed a significant association with increased DFS in this selected population of patients. This association was even higher in patients carrying both null-GSTT1 and -GSTM1 genotypes. The gene deletion of GSTs may predict not only the early onset of breast carcinoma but also the clinical response to chemotherapy and the recurrence-free survival for patients with lymph nodenegative breast carcinoma.

show abstract

“…The suggested causes of mitochondrial apoptotic pathway were initiated either by damaging stimuli such as oxidative stress (Berrigan et al, 1987;Venkatesan & Chandrakasan, 1995;Murata et al, 2004) or DNA damage by DNA alkylation (Gamcsik et al, 1999;Coppola & Ghibelli, 2000). While the oocytic organelles became scanty and haphazard in distribution, the mitochondria were either showing destructed cristae or appeared electron-dense (late sign of atretic oocyte).…”

Section: Electron Microscopic Resultsmentioning

confidence: 99%

Effect of Cyclophosphamide on the Postnatal Development of the Ovary of the Albino Rat

hassan

Zaghloul

Anwar

et al. 2011

The Egyptian Journal of Anatomy

View full text Add to dashboard Cite

Background: Cyclophosphamide is the most widely used alkylating agent in the treatment of haematological malignancies. On the other hand, cyclophosphamide has adverse effects on the fertility of both sexes. Aim of the work: The present work was done to study the histological and stereological changes in the developing ovary of the albino rat after a period of treatment with cyclophosphamide and the effect of rehabilitation after stopping the drug. Materials and Methods: Thirty-six immature female rats (newborn, one week, two weeks, oneand-half month and two-and-half month) were used in this study. They were subdivided into two groups. The control group (n=24) was injected intraperitoneally with dextrose 5%. The experimental group (n= 12) at the age of two weeks, received 100mg/ kg body weight cyclophosphamide intraperitoneally once weekly for four successive weeks. At the end of the treatment period this group was subdivided into two subgroups: subgroup A (treated group) including the rats at the age of one-andhalf month and subgroup B (rehabilitated group) including the rats at the age of two-and-half month which received the same drug regimen, but sacrificed after another four weeks without treatment. The specimens of all age groups were processed and stained with Heamatoxylin and Eosin. Other specimens at the age of one-and-half month were processed for semi-thin and ultra-thin examination. In the two age groups (control and treated) morphometeric measurements were performed. Results: The study showed shrinkage with decrease in the number and the size of the antral follicles, apoptosis and disorganization in the granulosa cell layers. Ultrastucturally, the most important feature observed was the fragmentation and leakage of the cellular nuclear materials of the granulosa cells and their clumping in the antrum. Morphometeric measurements showed a very highly significant reduction in the average follicular and oocytic diameter of the antral follicles and in the number of the healthy antral follicles while there was high significant reduction in the number of atretic antral follicles. In the rehabilitated group the follicles were less affected. Oocytes were affected in both groups; they were either vacuolated or totally absent. Morphometeric measurements showed highly significant reduction of the average oocytic diameter and in the average number of the granulosa cell layers.

show abstract

Modulation of cyclophosphamide-induced early lung injury by curcumin, an anti-inflammatory antioxidant

Cited by 86 publications

References 37 publications

Modulation of cyclophosphamide-induced early lung injury by allicin

Modulation of cyclophosphamide-induced early lung injury by allicin

Glutathione S-transferases (GSTT1 and GSTM1) gene deletions in Tunisians: susceptibility and prognostic implications in breast carcinoma

Effect of Cyclophosphamide on the Postnatal Development of the Ovary of the Albino Rat

Contact Info

Product

Resources

About