Gut glutathione metabolism and changes with 7,12-DMBA and glutamine

Johnson, Anita; Kaufmann, Yihong; Luo, Shaoke; Babb, Kirk; Hawk, Roger M.; Klimberg, V. Suzanne

doi:10.1016/j.jss.2003.07.003

Cited by 19 publications

(10 citation statements)

References 19 publications

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“…The effects of GLN on tumor development and tumor and gut mucosa GSH levels were presented and discussed elsewhere (4)(5)(6)(7)(8). The data showed that GLN supplementation reduced tumor development in the DMBA-breast cancer model by 50% to 75%, and this was associated with reduced tumor weight and volume (4,5).…”

Section: Resultsmentioning

confidence: 99%

“…We suggested that this block might lead to a decreased supply of the important antioxidant GSH at a time when it may be crucial for the prevention of oxidative damage produced by DMBA and at a place where most DMBA metabolism may be activated and further result in DNA adducts in the breast (6). It was also found that oral GLN restored the depressed gut GSH release, increased gut GSH concentration, and preserved normal gut structure (7). In addition, oral GLN significantly decreased tumor GSH level and further stimulated tumor apoptosis (8).…”

Section: Introductionmentioning

confidence: 92%

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Glutamine Affects Glutathione Recycling Enzymes in a DMBA-Induced Breast Cancer Model

Kaufmann

Тодорова

Luo

et al. 2008

Nutrition and Cancer

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Malignancy depletes host glutathione (GSH) levels to increase treatment-related toxicity and increases itself to resist the treatments. Our previous studies have shown that dietary glutamine (GLN) prevented 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumors through enhancing gut GSH release and reducing tumor GSH level. In addition, GSH synthesis, metabolism, and recycling are accomplished in gamma-glutamyl cycle. We hypothesized that the GLN prevention might be through a differential regulation of the gamma-glutamyl cycle enzymes. Female Sprague-Dawley rats were randomized into DMBA-tumor bearing, DMBA-treated, and control groups subdivided into GLN and water groups. GLN supplementation was given at 1 g/kg/day by gastric gavage. The activities and messenger RNA levels of gamma-glutamyl transpeptidase (GTP), gamma-glutamylcysteine synthetase (GCS), 5-oxo-L-prolinase (OPase), gamma-glutamyl transferase (GTF), and glutaminase (GLNase) were determined in gut mucosa and breast tumor using specific enzyme assays and semiquantitative reverse transcription polymerase chain reaction. GLN upregulated gut GTP, GCS, OPase, and GLNase in DMBA-tumor bearing, DMBA-treated, and/or control rats; however, it downregulated these enzymes in the tumor. The paradoxical effect of GLN on key GSH recycling enzymes in the gut versus tumor suggests that dietary supplemental GLN could be used in the clinical practice to increase the therapeutic index of cancer treatments by protecting normal tissues from, and sensitizing tumor cells to, chemotherapy and radiation-related injury.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

Glutamine Affects Glutathione Recycling Enzymes in a DMBA-Induced Breast Cancer Model

Kaufmann

Тодорова

Luo

et al. 2008

Nutrition and Cancer

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“…Glutathione is involved in several critical cellular defensive functions including free‐radical scavenging, detoxification of electrophiles, and maintenance of thiol‐disulfide status and signal transduction (Sen and Packer, 1996). It is well documented that Gln can provide intracellular glutamate as a substrate for GSH biosynthesis (Johnson et al., 2003; Alteheld et al., 2005; Wasa et al., 2005). The presence of high levels of organic GSH in fish also suggests that dietary supplementation with exogenous Gln enhances the synthesis of GSH as compared to that in the controls for whom this additional nutrition was not provided.…”

Section: Discussionmentioning

confidence: 99%

Dietary glutamine supplementation improves tissue antioxidant status and serum non-specific immunity of juvenile Hybrid sturgeon (Acipenser schrenckii ♀ × Huso dauricus♂)

Zhu

Hong

et al. 2011

Journal of Applied Ichthyology

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Exogenous glutamine (Gln) was evaluated for its effect on antioxidation and serum non-specific immunity in juvenile Hybrid sturgeon (Acipenser schrenckii $ · Huso dauricus #). Seven basal diets supplemented with 0.0, 0.3, 0.6, 0.9, 1.2, 1.5% of Gln and 1.0% alanyl-glutamine (Aln-Gln) were fed to fish (initial mean weight: 22.38 ± 0.18 g) for 8 weeks, and the experiment was conducted in triplicate. Treatment of fish supplemented with 1.2, 1.5% of Gln, or 1.0% of Aln-Gln caused a significantly higher glutathione peroxidase (GPX), superoxide dismutase (SOD) activities, and glutathione (GSH) content, and lower serum malondialdehyde (MDA) levels (P < 0.05) in serum, hepatopancreas and muscles. The addition of 0.9% Gln significantly improved the serum complement-3 (C3) and complement-4 (C4) levels (P < 0.05). These findings suggest that diet supplementation with 0.9-1.2% Gln or 1.0% of Aln-Gln may enhance the activity of the antioxidant defense system and the serum non-specific immunity of juvenile Hybrid sturgeon.

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“…Our laboratory has demonstrated that dietary Gln supplementation increased the intestinal weight and alkaline phosphosphate activity, and thus improved fish intestinal structure and function in Jian carp [24]. Furthermore, Gln serves as a metabolic precursor for glutathione (GSH) which can efficiently reduce ROS [25], [26]. It can protect fish enterocytes against H 2 O 2 -induced oxidative damage [27].…”

Section: Introductionmentioning

confidence: 99%

Soybean β-Conglycinin Induces Inflammation and Oxidation and Causes Dysfunction of Intestinal Digestion and Absorption in Fish

et al. 2013

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β-conglycinin has been identified as one of the major feed allergens. However, studies of β-conglycinin on fish are scarce. This study investigated the effects of β-conglycinin on the growth, digestive and absorptive ability, inflammatory response, oxidative status and gene expression of juvenile Jian carp (Cyprinus carpio var. Jian) in vivo and their enterocytes in vitro. The results indicated that the specific growth rate (SGR), feed intake, and feed efficiency were reduced by β-conglycinin. In addition, activities of trypsin, chymotrypsin, lipase, creatine kinase, Na+,K+-ATPase and alkaline phosphatase in the intestine showed similar tendencies. The protein content of the hepatopancreas and intestines, and the weight and length of the intestines were all reduced by β-conglycinin. β-conglycinin increased lipid and protein oxidation in the detected tissues and cells. However, β-conglycinin decreased superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and glutathione (GSH) content in the intestine and enterocytes. Similar antioxidant activity in the hepatopancreas was observed, except for GST. The expression of target of rapamycin (TOR) gene was reduced by β-conglycinin. Furthermore, mRNA levels of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) genes were increased by β-conglycinin. However, β-conglycinin increased CuZnSOD, MnSOD, CAT, and GPx1b gene expression. In conclusion, this study indicates that β-conglycinin induces inflammation and oxidation, and causes dysfunction of intestinal digestion and absorption in fish, and finally reduces fish growth. The results of this study provide some information to the mechanism of β-conglycinin-induced negative effects.

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Gut glutathione metabolism and changes with 7,12-DMBA and glutamine

Cited by 19 publications

References 19 publications

Glutamine Affects Glutathione Recycling Enzymes in a DMBA-Induced Breast Cancer Model

Glutamine Affects Glutathione Recycling Enzymes in a DMBA-Induced Breast Cancer Model

Dietary glutamine supplementation improves tissue antioxidant status and serum non-specific immunity of juvenile Hybrid sturgeon (Acipenser schrenckii ♀ × Huso dauricus♂)

Soybean β-Conglycinin Induces Inflammation and Oxidation and Causes Dysfunction of Intestinal Digestion and Absorption in Fish

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