Nicotine induces Nme2-mediated apoptosis in mouse testes

Gu, Yuwei; Xu, Wangjie; Nie, Dongsheng; Zhang, Dong; Dai, Jingbo; Zhao, Xianglong; Zhang, Meixing; Wang, Zhaoxia; Chen, Zhong; Qiao, Zhongdong

doi:10.1016/j.bbrc.2016.03.044

Cited by 18 publications

(15 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Accordingly, NIC adversely affected the Leydig cell as well as TDI, MI, SCI, and SPI indices. Our results were in agreement with previous studies . The previous observations also indicated that NIC‐induced germ cells degeneration may be the result of the low intra‐testicular concentrations of testosterone, which is essential for the normal spermatogenesis as well as the maintenance of structural morphology and normal physiology of the STs…”

Section: Discussionsupporting

confidence: 93%

“…20,47 In addition, NIC induces adverse effects in testicular functions through reducing mRNA and protein levels of Bcl-2 and upregulating the p53 and Caspase-3 mRNA and protein levels. 17 This study showed that NIC at both doses caused several histopathological changes at spermatogenesis level and diminished the testosterone content. Accordingly, NIC adversely affected the Leydig cell as well as TDI, MI, SCI, and SPI indices.…”

Section: Discussionmentioning

confidence: 67%

“…It is known that NIC increases the ROS production and induces oxidative stress via reduction in antioxidant enzyme activity in all tissues, especially in testis . In addition, NIC induces adverse effects in testicular functions through reducing mRNA and protein levels of Bcl‐2 and up‐regulating the p53 and Caspase‐3 mRNA and protein levels …”

Section: Discussionmentioning

confidence: 99%

“…In spite of the increased knowledge about the adverse effects of NIC on reproductive function, the actual molecular events resulting in male reproductive toxicity remain unclear. Currently, it is well known that NIC by declining the testosterone production, mRNA, and protein levels of Bcl‐2 reduction and up regulation of the p53 and Caspase‐3 mRNA and protein levels, adversely affects the spermatogenesis resulting in cellular depletion . Moreover, NIC leads to Nme2‐mediated apoptosis through inhibition of its up‐expression in mouse germ cells .…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Antioxidant and anti‐apoptotic effects of royal jelly against nicotine‐induced testicular injury in mice

Azad

Nejati

Jalali

et al. 2019

Environmental Toxicology

View full text Add to dashboard Cite

This study describes the effects of royal jelly (RJ) on testicular injury induced by nicotine (NIC) in mice. Thirty‐six male BALB/c mice were randomly divided into six groups (n = 6). Group 1 received normal saline, group 2 received 100 mg/kgBW/day RJ, groups 3 and 4 received NIC at doses of 0.50 and 1.00 mg/kgBW/day, respectively, and groups 5 and 6 received NIC at doses of 0.50 and 1.00 mg/kg BW/day, respectively, plus RJ. Following 35 days, the serum level of testosterone, histopathological changes, germ cell apoptosis, proliferating cell nuclear antigen (PCNA), malondialdehyde (MDA) content, and antioxidant indexes including total antioxidant capacity (TAC) and catalase (CAT) activity were determined. In addition, the mitochondria‐dependent apoptosis was investigated by assessing the Bcl‐2, p53, and Caspase‐3 mRNA levels expression by reverse transcription‐PCR (RT‐PCR). Compared to NIC receiving groups, the concomitant administration of RJ could protect the testosterone reduction and histological damages. After RJ treatment, the level of tissue MDA content decreased, while tissue TAC and CAT levels were remarkably increased compared to NIC‐exposed groups. Remarkable higher TUNEL‐positive germ cells and low PCNA index were observed in NIC receiving groups. Besides, the expression level of Bcl‐2 was significantly higher and the p53 and Caspase‐3 levels were significantly lower in the RJ co‐administration groups than NIC‐only receiving groups. Our results confirmed that RJ effectively protects the testis against NIC evoked damages by antioxidant and anti‐apoptotic effects involving the up regulation of the antioxidant status, mitochondria‐dependent apoptosis pathway prevention, and the proliferating activity improvement.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Antioxidant and anti‐apoptotic effects of royal jelly against nicotine‐induced testicular injury in mice

Azad

Nejati

Jalali

et al. 2019

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…These results indicate that nicotine doesn’t cause podocyte proliferation. Nicotine has also been reported to induce apoptosis in various cells [18, 47, 48]. Consistent with these reports, we found that nicotine increased the number of apoptotic cells and enhanced the expression of apoptotic protein markers including cleaved caspase-3.…”

Section: Discussionsupporting

confidence: 91%

Nicotine Induces Podocyte Apoptosis through Increasing Oxidative Stress

et al. 2016

View full text Add to dashboard Cite

BackgroundCigarette smoking plays an important role in the progression of chronic kidney disease (CKD). Nicotine, one of the major components of cigarette smoking, has been demonstrated to increase proliferation of renal mesangial cells. In this study, we examined the effect of nicotine on podocyte injury.MethodsTo determine the expression of nicotinic acetylcholine receptors (nAChR subunits) in podocytes, cDNAs and cell lysate of cultured human podocytes were used for the expression of nAChR mRNAs and proteins, respectively; and mouse renal cortical sections were subjected to immunofluorescant staining. We also studied the effect of nicotine on podocyte nephrin expression, reactive oxygen species (ROS) generation (via DCFDA loading followed by fluorometric analysis), proliferation, and apoptosis (morphologic assays). We evaluated the effect of nicotine on podocyte downstream signaling including phosphorylation of ERK1/2, JNK, and p38 and established causal relationships by using respective inhibitors. We used nAChR antagonists to confirm the role of nicotine on podocyte injury.ResultsHuman podocytes displayed robust mRNA and protein expression of nAChR in vitro studies. In vivo studies, mice renal cortical sections revealed co-localization of nAChRs along with synaptopodin. In vitro studies, nephrin expression in podocyte was decreased by nicotine. Nicotine stimulated podocyte ROS generation; nonetheless, antioxidants such as N-acetyl cysteine (NAC) and TEMPOL (superoxide dismutase mimetic agent) inhibited this effect of nicotine. Nicotine did not modulate proliferation but promoted apoptosis in podocytes. Nicotine enhanced podocyte phosphorylation of ERK1/2, JNK, and p38, and their specific inhibitors attenuated nicotine-induced apoptosis. nAChR antagonists significantly suppressed the effects of nicotine on podocyte.ConclusionsNicotine induces podocyte apoptosis through ROS generation and associated downstream MAPKs signaling. The present study provides insight into molecular mechanisms involved in smoking associated progression of chronic kidney disease.

show abstract

Testing for paternal influences on offspring telomere length in a human cohort in the Philippines

Eisenberg

Rej

Duazo

et al. 2019

American J Phys Anthropol

View full text Add to dashboard Cite

Objectives: Telomeres, emerging biomarkers of aging, are comprised of DNA repeats located at chromosomal ends that shorten with cellular replication and age in most human tissues. In contrast, spermatocyte telomeres lengthen with age. These changes in telomere length (TL) appear to be heritable, as older paternal ages of conception (PAC) predict longer offspring TL. Mouse-model studies raise questions about the potential for effects of paternal experiences on human offspring TL, as they suggest that smoking, inflammation, DNA damage, and stressors all shorten sperm TL. Here, we examined whether factors from the paternal environment predict offspring TL as well as interact with PAC to predict offspring TL.Materials and Methods: Using data from the Philippines, we tested if smoking, psychosocial stressors, or shorter knee height (a measure of early life adversity) predict shorter offspring TL. We also tested if these interacted with PAC in predicting offspring TL.Results: While we did not find the predicted associations, we observed a trend toward fathers with shorter knee height having offspring with longer TL. In addition, we found that knee height interacted with PAC to predict offspring TL. Specifically, fathers with shorter knee heights showed a stronger positive effect of PAC on offspring TL.Discussion: While the reasons for these associations remain uncertain, shorter knee height is characteristic of earlier puberty. Since spermatocyte TL increases with the production of sperm, we speculate that individuals with earlier puberty, and its concomitant commencement of production of sperm, had more time to accumulate longer sperm telomeres. K E Y W O R D Sepigenetics, intergenerational effects, intergenerational inertia, intergenerational plasticity, senescence

show abstract

Nicotine induces Nme2-mediated apoptosis in mouse testes

Cited by 18 publications

References 19 publications

Antioxidant and anti‐apoptotic effects of royal jelly against nicotine‐induced testicular injury in mice

Antioxidant and anti‐apoptotic effects of royal jelly against nicotine‐induced testicular injury in mice

Nicotine Induces Podocyte Apoptosis through Increasing Oxidative Stress

Testing for paternal influences on offspring telomere length in a human cohort in the Philippines

Contact Info

Product

Resources

About