Diabetes-induced DNA damage and apoptosis are associated with poly (ADP ribose) polymerase 1 inhibition in the rat testis

Narayana, K.; Al‐Hussaini, Heba; Al‐Bader, Maie

doi:10.1016/j.ejphar.2014.05.005

Cited by 60 publications

(50 citation statements)

References 53 publications

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“…Expression of PARP1 was evaluated in Leydig cells and in intra-testicular blood vessels. Stage-dependent expression of PARP1 and SirT1 was also analyzed [2].Data format Analyzed Experimental factors Adult 13–15 week-old male Wistar rats were used. Diabetes was induced by Streptozotocin injection.…”

mentioning

confidence: 99%

Dataset of Trans-Resveratrol on diabetes-induced abnormal spermatogenesis, poly (ADP-ribose) polymerase-1 (PARP1) expression in intra-testicular blood vessels, and stage-dependent expression of PARP1 and Sirtuin 1 in the rat testis

2017

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This article contains data related to the article “Effects of Trans-Resveratrol on hyperglycemia-induced abnormal spermatogenesis, DNA damage and alterations in poly (ADP-ribose) polymerase signaling in rat testis” (A. Abdelali, M. Al-Bader, N. Kilarkaje, 2016) [1]. The data are related to Resveratrol on diabetes-induced changes in blood glucose levels, body weights of rats, sperm count and motility, expression of poly (ADP-ribose) polymerase-1 (PARP1) in Leydig cells and in intratesticular blood vessels, and stage-dependent expression of PARP1 and Sirtuin 1 (SirT1) in the rat testis. In this experiment, the data were obtained from control, Resveratrol-treated, diabetic and Resveratrol-treated diabetic rats on day 42 after the induction of diabetes. Resveratrol treatment for a group each of normal and diabetic rats started on day 22 and extended up to day 42. The sperm parameters were conducted in samples obtained from the epididymis. The expression of proteins was evaluated by immunohistochemistry by using specific primary antibodies. The data are presented in the form of figures and significance of them has been given in the research article [1].

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mentioning

confidence: 99%

Dataset of Trans-Resveratrol on diabetes-induced abnormal spermatogenesis, poly (ADP-ribose) polymerase-1 (PARP1) expression in intra-testicular blood vessels, and stage-dependent expression of PARP1 and Sirtuin 1 in the rat testis

2017

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“…Animal studies have shown that diabetes increases the levels of the oxidative DNA damage marker 8-oxo-dG in the rat renal cortex[25, 26], testis[27], and corpus cavernosum[28]. However, the extent of DNA damage in diabetes-associated embryos remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Maternal diabetes triggers DNA damage and DNA damage response in neurulation stage embryos through oxidative stress

Dong

et al. 2015

Biochemical and Biophysical Research Communications

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DNA damage and DNA damage response (DDR) in neurulation stage embryos under maternal diabetes conditions are not well understood. The purpose of this study was to investigate whether maternal diabetes and high glucose in vitro induce DNA damage and DDR in the developing embryo through oxidative stress. In vivo experiments were conducted by mating superoxide dismutase 1 (SOD1) transgenic male mice with wild-type (WT) female mice with or without diabetes. Embryonic day 8.75 (E8.75) embryos were tested for the DNA damage markers, phosphorylated histone H2A.X (p-H2A.X) and DDR signaling intermediates, including phosphorylated checkpoint 1 (p-Chk1), phosphorylated checkpoint 2 (p-Chk2), and p53. Levels of the same DNA damage markers and DDR signaling intermediates were also determined in the mouse C17.2 neural stem cell line. Maternal diabetes and high glucose in vitro significantly increased the levels of p-H2A.X. Levels of p-Chk1, p-Chk2, and p53, were elevated under both maternal diabetic and high glucose conditions. SOD1 overexpression blocked maternal diabetes-induced DNA damage and DDR in vivo. Tempol, a SOD1 mimetic, diminished high glucose-induced DNA damage and DDR in vitro. In conclusion, maternal diabetes and high glucose in vitro induce DNA damage and activates DDR through oxidative stress, which may contribute to the pathogenesis of diabetes-associated embryopathy.

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“…These results are similar to those of previous reports. (24,25) The free radicals produced by the normal metabolic processes are maintained in balance by endogenous and exogenous antioxidants that act as free radical scavengers. Oxidative stress occurs when the concentration of free radicals exceeds the detoxifying capacity of cellular antioxidants.…”

Section: Christijanti Marianti Isnaenimentioning

confidence: 99%

Aloe vera extract reduces 8-oxo-2'-deoxyguanosine levels and improves total antioxidants in streptozotocin-induced diabetic rats

Christijanti

Marianti

Isnaeni

2017

UnivMed

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BACKGROUNDDiabetes mellitus is a chronic disease caused by lack of insulin production in the pancreas or by insulin resistance, the disease being characterized by elevated blood glucose levels. Hyperglycemia in diabetes could lead to oxidative stress due to the rise in 8-oxo-2'-deoxyguanosine (8-oxo-dG) levels and the decrease in levels of total antioxidant status (TAS). The purpose of this study was to assess the effect Aloe vera extract on 8-oxodG level and total antioxidant status in diabetic rat testis.

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Diabetes-induced DNA damage and apoptosis are associated with poly (ADP ribose) polymerase 1 inhibition in the rat testis

Cited by 60 publications

References 53 publications

Dataset of Trans-Resveratrol on diabetes-induced abnormal spermatogenesis, poly (ADP-ribose) polymerase-1 (PARP1) expression in intra-testicular blood vessels, and stage-dependent expression of PARP1 and Sirtuin 1 in the rat testis

Dataset of Trans-Resveratrol on diabetes-induced abnormal spermatogenesis, poly (ADP-ribose) polymerase-1 (PARP1) expression in intra-testicular blood vessels, and stage-dependent expression of PARP1 and Sirtuin 1 in the rat testis

Maternal diabetes triggers DNA damage and DNA damage response in neurulation stage embryos through oxidative stress

Aloe vera extract reduces 8-oxo-2'-deoxyguanosine levels and improves total antioxidants in streptozotocin-induced diabetic rats

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