Effects of Progesterone on Benzene Toxicity in Rats

Verma, Yeshvandra; Rana, S. V. S.

doi:10.2478/10004-1254-59-2008-1835

Cited by 13 publications

(9 citation statements)

References 25 publications

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“…On the other hand, Cheng et al (2006) obtained the opposite results using hepatoma HuH-7 cells, indicating that the beneficial or deleterious effects of this hormone may be tissue-specific. Though the mechanism of progesterone cytotoxicity is not completely clarified, the ability of progesterone to induce oxidative stress has been investigated (Verma & Rana 2008).…”

Section: Discussionmentioning

confidence: 99%

Progesterone induces apoptosis of insulin-secreting cells: insights into the molecular mechanism

Nunes¹,

Portioli-Sanches²,

Rosim³

et al. 2014

Journal of Endocrinology

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Progesterone has been associated with the development of gestational diabetes (GD) due to the enhancement of insulin resistance. As b-cell apoptosis participates in type 1 and type 2 diabetes pathophysiology, we proposed the hypothesis that progesterone might contribute to the development of GD through a mechanism that also involves b-cell death. To address this question, RINm5F insulin-producing cells were incubated with progesterone (25-100 mM), in the presence or absence of a-tocopherol (40 mM). After 24 or 48 h, membrane integrity and DNA fragmentation were analyzed by flow cytometry. Caspase activity was used to identify the mode of cell death. The involvement of endoplasmic reticulum stress in the action of progesterone was investigated by western blotting. Oxidative stress was measured by 2',7'-dichlorofluorescein diacetate (DCFDA) oxidation. Isolated rat islets were used in similar experiments in order to confirm the effect of progesterone in primary b-cells. Incubation of RINm5F cells with progesterone increased the number of cells with loss of membrane integrity and DNA fragmentation. Progesterone induced generation of reactive species. Pre-incubation with a-tocopherol attenuated progesterone-induced apoptosis. Western blot analyses revealed increased expression of CREB2 and CHOP in progesteronetreated cells. Progesterone caused apoptotic death of rat islet cells and enhanced generation of reactive species. Our results show that progesterone can be toxic to pancreatic b-cells through an oxidative-stress-dependent mechanism that induces apoptosis. This effect may contribute to the development of GD during pregnancy, particularly under conditions that require administration of pharmacological doses of this hormone.

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Section: Discussionmentioning

confidence: 99%

Progesterone induces apoptosis of insulin-secreting cells: insights into the molecular mechanism

Nunes¹,

Portioli-Sanches²,

Rosim³

et al. 2014

Journal of Endocrinology

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“…Regarding progesterone effects on different cell types, Verma and Rana [ 15 ] found high lipid peroxidation in the liver and kidneys of benzene-treated rats after receiving doses of this hormone. Cheng et al [ 16 ] have demonstrated that progesterone was capable of contributing to TNF- α -mediated apoptosis by a mechanism involving the generation of free radicals in HuH-7 hepatoma cells.…”

Section: Introductionmentioning

confidence: 99%

Vitamins Modulate the Expression of Antioxidant Genes in Progesterone-Treated Pancreatic β Cells: Perspectives for Gestational Diabetes Management

Borçari

Santos

Reigado

et al. 2020

International Journal of Endocrinology

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Gestational diabetes (GD) is a condition defined as carbohydrate intolerance and hyperglycemia beginning in the second trimester of pregnancy, which overlaps with the progesterone exponential increase. Progesterone has been shown to cause pancreatic β-cell death by a mechanism dependent on the generation of reactive oxygen species and oxidative stress. Herein, we studied the effect of this hormone on the expression of 84 genes related to oxidative stress and oxidant defense in pancreatic RINm5F cell lineage. Cells were incubated with 0.1, 1.0, or 100 μM progesterone for 6 or 24 h, in the presence or absence of the vitamins E and C. Among the investigated genes, five of them had their expression increased, at least 2-fold, in two different concentrations independently of the time of incubation, or at the same concentration at the different time points, including those that encode for stearoyl-CoA desaturase 1 (Scd1), dual oxidase 1 (Duox1), glutathione peroxidase 6 (GPx6), heme oxygenase 1 (Hmox1), and heat shock protein a1a (Hspa1a). Vitamins E and C were able to increase, in progesterone-treated cells, the expression of genes with antioxidant function such as Hmox1, but decreased Scd1 expression, a gene with prooxidant function. At cytoplasmic level, progesterone positively modulated Hmox1 and Hspa1a content. These results suggest that the protein encoded by these genes might protect cells against progesterone induced-oxidative damage, opening perspectives to elucidate the molecular mechanism involved in progesterone action in GD, as well as for the development of antioxidant strategies for the prevention and treatment of this disease.

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“…By these mechanisms, progesterone could prevent cellular apoptosis also in brain and heart tissues [5][6][7][8][9] . Building on these findings we performed a study aimed at evaluating the protective effect of treatment with progesterone in the TNBS-induced colitis rat model.…”

Section: Introductionmentioning

confidence: 99%

The effect of progesterone in the prevention of the chemically induced experimental colitis in rats

Karatepe¹,

Altıok²,

Battal³

et al. 2012

Acta Cir. Bras.

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PURPOSE:To study the effects of progesterone on an experimental colitis model. METHODS:Wistar albino rats were treated subcutaneously with 2mg/kg once a day during seven days Colitis was induced by intrarectal administration of 5mg trinitrobenzene sulfonic acid (TNBS). Disease activities, macroscopic and microscopic scores were evaluated.To determine the response provoked by progesterone we measured Colonic malondialdehyde (MDA), TNF alfa, IL-6 and Nitric oxide (NO) levels in addition to the MPO (Myeloperoxidase) and caspase-3 activities. RESULTS:Progesterone ameliorated significantly the macroscopic and microscopic scores. TNBS-induced colitis significantly increased the colonic MDA levels and caspase-3 activities in group 2 in comparison to the control group. The results of the study revealed a decline in MDA, NO, IL6 and TNF-α levels in the colon tissue and in blood due to progesterone therapy in group 3 when compared to the group 2, a significant improvement. Progesterone treatment was associated with decreased MDA, MPO, TNF alfa and caspase-3 activity. CONCLUSION:Progesterone therapy decreased oxidative damage in the colonic mucosa.Key words: Progesterone. Colitis. Inflammation. Colon. Rats. RESUMO OBJETIVO:Investigar os efeitos da progesterona em um modelo de colite experimental. MÉTODOS:Ratos albinos Wistar foram tratados subcutaneamente com 2mg/kg por dia durante sete dias. A colite foi induzida por administração intrarretal de 5mg ácido sulfônico trinitrobenzeno (TNBS). Foram avaliadas as atividades da doença, escores macroscópicos e microscópicos Para determinar a resposta provocada pela progesterona foi medida no cólon os níveis de malondialdeído (MDA), TNF alfa, IL-6 e óxido nítrico (NO), além da atividade da MPO (Myeloperoxidase) e caspase-3. RESULTADOS:A progesterone melhorou significantemente os escores macroscópicos e microscópicos. A colite induzida pelo TNBS significantemente aumentou os níveis colônicos de MDA e a atividade da caspase-3 no grupo 2 em comparação com o grupo controle.Os resultados do estudo revelaram um declínio nos níveis de MDA, NO, IL6 e TNF-α no tecido colônico e no sangue devido à terapia com a progesterona no grupo 3 quando comparado ao grupo 2. O tratamento com a progesterona foi associado com decréscimo do MDA, MPO, TNF alfa e atividade da caspase-3. CONCLUSÃO:A terapia com progesterona decresce o dano oxidativo na mucosa do cólon.Descritores: Progesterona. Colite. Inflamação. Colo. Ratos.Karatepe O et al.

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Effects of Progesterone on Benzene Toxicity in Rats

Cited by 13 publications

References 25 publications

Progesterone induces apoptosis of insulin-secreting cells: insights into the molecular mechanism

Progesterone induces apoptosis of insulin-secreting cells: insights into the molecular mechanism

Vitamins Modulate the Expression of Antioxidant Genes in Progesterone-Treated Pancreatic β Cells: Perspectives for Gestational Diabetes Management

The effect of progesterone in the prevention of the chemically induced experimental colitis in rats

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