Chemoprotective effect of ascorbic acid, α-tocopherol, and selenium on cyclophosphamide-induced toxicity in the rat ovarium

Gürgen, Seren Gülşen; Erdoğan, Deniz; Elmas, Çiğdem; Kaplanoğlu, Gülnur Take; Özer, Çiğdem

doi:10.1016/j.nut.2012.11.004

Cited by 38 publications

(31 citation statements)

References 32 publications

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“…The concentration of the PCNA We found that vitamin C coadministrattion enhances the effect of nicotine in the liver and kidney through increasing PCNA expression significantly in both tissues. In agreement with our results Gürgen and his colleagues suggested that ascorbic acid through increasing PCNA expression reduced the cyclophosphamideinduced damage of rat ovarian tissue [57]. Another study showed that coadministration of ascorbic acid and kojic acid increased the number of liver cells positive for PCNA and reduced the number of TUNEL-positive cells probably through its antioxidant activity [58].…”

Section: Discussionsupporting

confidence: 91%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

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Abstract:Objective: Vitamin Methods: Animals were divided into four groups; (C) saline-treated, (VC) vitamin C-treated, (NIC) nicotinetreated, all were for 3 weeks, and (NIC+VC) is given vitamin C for 3 days prior, with nicotine injection and 2 days thereafter. Results: Present work showed that nicotine exposure caused significant reduction in total body weight, relative liver and kidney weights, elevated malondialdehyde (MDA), alanine transaminase (ALT), aspirate transaminase (AST), and alkaline phosphatase (ALP) in both hepatic and renal tissues. Co-exposure to nicotine and vitamin C maintained normal liver and kidney weight, significantly lowered MDA, ALT, AST, ALP and elevated glutathione in both hepatic and renal tissues compared NIC group as well as controls. Nicotine administration resulted in shedding, necrosis, and loss of brush border of cells covering proximal and distal convoluted tubules of kidney. The liver in the nicotine-treated group showed vacuolated cytoplasm of hepatocytes, with dilated central vein and sinusoids and mitochondrial destruction. Immunohistochemistry showed dense PCNA immunostaining in the livers of nicotine-treated rats. Vitamin C induced partial correction of nicotine-induced histopathological damage of liver and kidney and significant elevation in PCNA expression. Conclusion:The results of present work suggested that vitamin C has a promising prophylactic effect against nicotine-induced oxidative damage of liver and kidney.

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Section: Discussionsupporting

confidence: 91%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

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“…For instance, thiol antioxidants (GSH-E and dithiothreitol) completely protected COV434 granulosa cell lines exposed to 4-HC while ascorbic acid (thiol unrelated) provided only minor benefit (43). On the other hand, thiol unrelated antioxidants such as ascorbic acid and vitamin E have been described as preventing cyclophosphamide-induced ovary (44) and hepatic (45) toxicity in rats, indicating context dependent differences. Thus, it should be noted that long-term and tissue specific in vivo effects of alkylating agents upon oxidative stress may have more relevance and should not be discounted.…”

Section: Discussionmentioning

confidence: 99%

Alkylating Agent–Induced NRF2 Blocks Endoplasmic Reticulum Stress–Mediated Apoptosis via Control of Glutathione Pools and Protein Thiol Homeostasis

Zanotto-Filho

Masamsetti

Loranc³

et al. 2016

Molecular Cancer Therapeutics

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Alkylating agents are a commonly used cytotoxic class of anticancer drugs. Understanding the mechanisms whereby cells respond to these drugs is key to identify means to improve therapy while reducing toxicity. By integrating genome-wide gene expression profiling, protein analysis and functional cell validation, we herein demonstrated a direct relationship between NRF2 and Endoplasmic Reticulum (ER) stress pathways in response to alkylating agents, which is coordinated by the availability of glutathione (GSH) pools. GSH is essential for both drug detoxification and protein thiol homeostasis within the ER, thus inhibiting ER stress induction and promoting survival; an effect independent of its antioxidant role. NRF2 accumulation induced by alkylating agents resulted in increased GSH synthesis via GCLC/GCLM enzyme, and interfering with this NRF2 response by either NRF2 knockdown or GCLC/GCLM inhibition with buthionine sulfoximine (BSO) caused accumulation of damaged proteins within the ER, leading to PERK-dependent apoptosis. Conversely, upregulation of NRF2, through KEAP1 depletion or NRF2-myc overexpression, or increasing GSH levels with N-acetylcysteine (NAC) or glutathione-ethyl-ester (GSH-E), decreased ER stress and abrogated alkylating agents-induced cell death. Based on these results, we identified a subset of lung and head-and-neck carcinomas with mutations in either KEAP1 or NRF2/NFE2L2 genes that correlate with NRF2 targets overexpression and poor survival. In KEAP1 mutant cancer cells, NRF2 knockdown and GSH depletion increased cell sensitivity via ER stress induction in a mechanism specific to alkylating drugs. Overall, we show that the NRF2-GSH influence on ER homeostasis implicates defects in NRF2-GSH or ER stress machineries as affecting alkylating therapy toxicity.

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“…Labeling intensity was graded semiquantitatively, and the HSCORE was calculated using the formula HSCORE = Σ Pi ( i + 1), where i is the intensity of labeling with a value of 1, 2, or 3 (weak, moderate, or strong, resp.) and Pi is the percentage of labeled epithelial and stromal cells for each intensity, within a range of 0–100% [24]. …”

Section: Methodsmentioning

confidence: 99%

A Comparison Study of Growth Factor Expression following Treatment with Transcutaneous Electrical Nerve Stimulation, Saline Solution, Povidone-Iodine, and Lavender Oil in Wounds Healing

Kutlu

Çeçen

Gürgen

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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This study compared the effects of transcutaneous electrical nerve stimulation (TENS), saline solution (SS), povidone-iodine (PI), and lavender oil (Lavandula angustifolia) through expression of growth factors in a rat model of wound healing. Six experimental groups were established, each containing 8 rats: a healthy group with no incision wounds, an incision-control group, an incision and TENS group, an incision and SS group, an incision and PI group, and an incision and lavender oil group. Experiments continued for 5 days, after which the skin in the excision area was removed. Tissue concentrations of epidermal growth factor (EGF) and platelet-derived growth factor (PDGF)-A were measured using enzyme-linked immunosorbent assay (ELISA). Tissue expressions of EGF, PDGF-A, and fibroblast growth factor (FGF)-2 were determined using immunohistochemistry. Wound closure progressed more rapidly in the TENS and lavender oil groups than in the control and other study groups. In particular, PDGF-A expressions in the dermis and EGF expression in the epidermis were significantly intense in the TENS group (P < 0.05). In addition, ELISA levels of growth factors such as PDGF-A and EGF were significantly higher in TENS group compared to the control group (P < 0.05). These immunohistochemical and ELISA results suggest that TENS may improve wound healing through increasing growth factors in the dermis and epidermis more than other topical applications.

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Chemoprotective effect of ascorbic acid, α-tocopherol, and selenium on cyclophosphamide-induced toxicity in the rat ovarium

Cited by 38 publications

References 32 publications

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Alkylating Agent–Induced NRF2 Blocks Endoplasmic Reticulum Stress–Mediated Apoptosis via Control of Glutathione Pools and Protein Thiol Homeostasis

A Comparison Study of Growth Factor Expression following Treatment with Transcutaneous Electrical Nerve Stimulation, Saline Solution, Povidone-Iodine, and Lavender Oil in Wounds Healing

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