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Induction of omega 6 inflammatory pathway by sodium metabisulfite in rat liver and its attenuation by ghrelin.

Ercan S, Kencebay C, Basaranlar G, Ozcan F, Derin N, Aslan M - Lipids Health Dis (2015)

Bottom Line: Tissue activity of COX and PGE2 levels were also significantly increased in liver tissue of sodium metabisulfite treated rats compared to controls.Ghrelin treatment decreased n-6 PUFA levels and reduced COX and PGE2 levels in liver tissue of sodium metabisulfite treated rats.Current results suggest that ghrelin exerts anti-inflammatory action through modulation of n-6 PUFA levels in hepatic tissue.

View Article: PubMed Central - PubMed

Affiliation: Akdeniz University, Vocational School of Health Services, Antalya, 07070, Turkey. sevimercan@akdeniz.edu.tr.

ABSTRACT

Background: Sodium metabisulfite is commonly used as preservative in foods but can oxidize to sulfite radicals initiating molecular oxidation. Ghrelin is a peptide hormone primarily produced in the stomach and has anti-inflammatory effects in many organs. This study aimed to assess endogenous omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) in rat peripheral organs following sodium metabisulfite treatment and determine the possible effect of ghrelin on changes in n-6 inflammatory pathway.

Methods: Male Wistar rats included in the study were allowed free access to standard rat chow. Sodium metabisulfite was given by gastric gavage and ghrelin was administered intraperitoneally for 5 weeks. Levels of arachidonic acid (AA, C20:4n-6), dihomo-gamma-linolenic acid (DGLA, C20:3n-6), eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3) in liver, heart and kidney tissues were determined by an optimized multiple reaction monitoring (MRM) method using ultra fast-liquid chromatography (UFLC) coupled with tandem mass spectrometry (MS/MS). Cyclooxygenase (COX) and prostaglandin E2 (PGE2) were measured in tissue samples to evaluate changes in n-6 inflammatory pathway.

Results: Omega-6 PUFA levels, AA/DHA and AA/EPA ratio were significantly increased in liver tissue following sodium metabisulfite treatment compared to controls. No significant change was observed in heart and kidney PUFA levels. Tissue activity of COX and PGE2 levels were also significantly increased in liver tissue of sodium metabisulfite treated rats compared to controls. Ghrelin treatment decreased n-6 PUFA levels and reduced COX and PGE2 levels in liver tissue of sodium metabisulfite treated rats.

Conclusion: Current results suggest that ghrelin exerts anti-inflammatory action through modulation of n-6 PUFA levels in hepatic tissue.

No MeSH data available.


Distribution of polyunsaturated fatty acids in the liver of experimental groups. C, control; S, sodium metabisulfite; G, ghrelin; S + G, sodium metabisulfite + ghrelin. DGLA, Dihomo-gamma-linolenic acid; AA, Arachidonic acid; EPA, Eicosapentaenoic acid; DHA, Docosahexaenoic acid.
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Fig3: Distribution of polyunsaturated fatty acids in the liver of experimental groups. C, control; S, sodium metabisulfite; G, ghrelin; S + G, sodium metabisulfite + ghrelin. DGLA, Dihomo-gamma-linolenic acid; AA, Arachidonic acid; EPA, Eicosapentaenoic acid; DHA, Docosahexaenoic acid.

Mentions: Levels of endogenous PUFAs measured in liver, heart and kidney tissues are given in Tables 1, 2 and 3, respectively. DGLA and AA levels were increased in liver tissue following sodium metabisulfite treatment compared to control and ghrelin treated groups. No significant change was observed in liver EPA and DHA amount following sodium metabisulfite treatment. Ghrelin treatment significantly decreased DGLA and AA levels in sodium metabisulfite treated rats. AA/DHA and AA/EPA ratio were significantly increased in liver tissue following sodium metabisulfite treatment compared to control, ghrelin and Na2S2O5 + ghrelin groups (Table 1). No significant change was observed in heart and kidney PUFA levels, AA/DHA and AA/EPA ratio (tables 2 and 3, respectively). Box plot graph data of AA (C20:4n-6), DGLA (C20:3n-6), EPA (C20:5n-3) and DHA (C22:6n-3) distribution in liver of all experimental groups are shown in Figure 3. The boundary of the box closest to zero indicates the 25th percentile, the line within the box marks the median, and the boundary of the box farthest from zero indicates the 75th percentile. Whiskers above and below the box indicate the 90th and 10th percentiles.Table 1


Induction of omega 6 inflammatory pathway by sodium metabisulfite in rat liver and its attenuation by ghrelin.

Ercan S, Kencebay C, Basaranlar G, Ozcan F, Derin N, Aslan M - Lipids Health Dis (2015)

Distribution of polyunsaturated fatty acids in the liver of experimental groups. C, control; S, sodium metabisulfite; G, ghrelin; S + G, sodium metabisulfite + ghrelin. DGLA, Dihomo-gamma-linolenic acid; AA, Arachidonic acid; EPA, Eicosapentaenoic acid; DHA, Docosahexaenoic acid.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4335696&req=5

Fig3: Distribution of polyunsaturated fatty acids in the liver of experimental groups. C, control; S, sodium metabisulfite; G, ghrelin; S + G, sodium metabisulfite + ghrelin. DGLA, Dihomo-gamma-linolenic acid; AA, Arachidonic acid; EPA, Eicosapentaenoic acid; DHA, Docosahexaenoic acid.
Mentions: Levels of endogenous PUFAs measured in liver, heart and kidney tissues are given in Tables 1, 2 and 3, respectively. DGLA and AA levels were increased in liver tissue following sodium metabisulfite treatment compared to control and ghrelin treated groups. No significant change was observed in liver EPA and DHA amount following sodium metabisulfite treatment. Ghrelin treatment significantly decreased DGLA and AA levels in sodium metabisulfite treated rats. AA/DHA and AA/EPA ratio were significantly increased in liver tissue following sodium metabisulfite treatment compared to control, ghrelin and Na2S2O5 + ghrelin groups (Table 1). No significant change was observed in heart and kidney PUFA levels, AA/DHA and AA/EPA ratio (tables 2 and 3, respectively). Box plot graph data of AA (C20:4n-6), DGLA (C20:3n-6), EPA (C20:5n-3) and DHA (C22:6n-3) distribution in liver of all experimental groups are shown in Figure 3. The boundary of the box closest to zero indicates the 25th percentile, the line within the box marks the median, and the boundary of the box farthest from zero indicates the 75th percentile. Whiskers above and below the box indicate the 90th and 10th percentiles.Table 1

Bottom Line: Tissue activity of COX and PGE2 levels were also significantly increased in liver tissue of sodium metabisulfite treated rats compared to controls.Ghrelin treatment decreased n-6 PUFA levels and reduced COX and PGE2 levels in liver tissue of sodium metabisulfite treated rats.Current results suggest that ghrelin exerts anti-inflammatory action through modulation of n-6 PUFA levels in hepatic tissue.

View Article: PubMed Central - PubMed

Affiliation: Akdeniz University, Vocational School of Health Services, Antalya, 07070, Turkey. sevimercan@akdeniz.edu.tr.

ABSTRACT

Background: Sodium metabisulfite is commonly used as preservative in foods but can oxidize to sulfite radicals initiating molecular oxidation. Ghrelin is a peptide hormone primarily produced in the stomach and has anti-inflammatory effects in many organs. This study aimed to assess endogenous omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) in rat peripheral organs following sodium metabisulfite treatment and determine the possible effect of ghrelin on changes in n-6 inflammatory pathway.

Methods: Male Wistar rats included in the study were allowed free access to standard rat chow. Sodium metabisulfite was given by gastric gavage and ghrelin was administered intraperitoneally for 5 weeks. Levels of arachidonic acid (AA, C20:4n-6), dihomo-gamma-linolenic acid (DGLA, C20:3n-6), eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3) in liver, heart and kidney tissues were determined by an optimized multiple reaction monitoring (MRM) method using ultra fast-liquid chromatography (UFLC) coupled with tandem mass spectrometry (MS/MS). Cyclooxygenase (COX) and prostaglandin E2 (PGE2) were measured in tissue samples to evaluate changes in n-6 inflammatory pathway.

Results: Omega-6 PUFA levels, AA/DHA and AA/EPA ratio were significantly increased in liver tissue following sodium metabisulfite treatment compared to controls. No significant change was observed in heart and kidney PUFA levels. Tissue activity of COX and PGE2 levels were also significantly increased in liver tissue of sodium metabisulfite treated rats compared to controls. Ghrelin treatment decreased n-6 PUFA levels and reduced COX and PGE2 levels in liver tissue of sodium metabisulfite treated rats.

Conclusion: Current results suggest that ghrelin exerts anti-inflammatory action through modulation of n-6 PUFA levels in hepatic tissue.

No MeSH data available.