Ethanol Exposure Enhances Apoptosis Within the Testes

Zhu, Qianlong; Meisinger, Jeremy; Emanuele, Nicholas V.; Emanuele, Mary Ann; LaPaglia, Nancy; Thiel, David H. Van

doi:10.1111/j.1530-0277.2000.tb04574.x

Cited by 69 publications

(48 citation statements)

References 62 publications

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“…In addition, numerous studies showed that apoptosis was an important mechanism by which ethanol caused tissue injury [27,28]. Recently, Zhu et al firstly showednumerous studies showed that apoptosis was an important mechanism by which ethanol caused tissue injury that chronic ethanol exposure enhanced apoptosis of testicular germ cells and measured expression of some apoptosis-related proteins such as Bcl-2, p53 and Fas ligand [19]. During the time of writing this paper, Eid et al suggested that Fas system might involve in germ cell apoptosis in rats treated with chronic ethanol for 12 weeks [29].…”

Section: Discussionmentioning

confidence: 99%

“…One is that ethanol metabolism produces an oxidative stress within the testes [15]; another is that ethanol exposure changes either testosterone [16] or esterone levels [17]. In addition, Zhu et al showed that ethanol exposure adversely affected the secretory function of Sertoli cells [18] and their recent research revealed enhanced apoptosis within the testes after chronic ethanol exposure [19]. However, it is still not clear how ethanol can lead to testicular injury.…”

Section: Introductionmentioning

confidence: 99%

“…However, it is still not clear how ethanol can lead to testicular injury. Recently, Zhu et al mentioned that the expression of Fas ligand and p53 within the testes were enhanced after chronic ethanol exposure [19], but no further evidences were provided.…”

Section: Introductionmentioning

confidence: 99%

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Enhancement of germ cell apoptosis induced by ethanol in transgenic mice overexpressing Fas Ligand

Jiang

Hua

et al. 2003

Cell Res

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It was suggested that chronic ethanol exposure could result in testicular germ cell apoptosis, but the mechanism is still unclear. In the present study, we use a model of transgenic mice ubiquitously overexpressing human FasL to investigate whether Fas ligand plays a role in ethanol-induced testicular germ cell apoptosis. Both wild-type (WT) mice and transgenic (TG) mice were treated with acute ethanol (20% v/v) by introperitoneal injection for five times. After ethanol injection, WT mice displayed up-regulation of Fas ligand in the testes, which was shown by FITCconjugated flow cytometry and western blotting. Moreover, TG mice exhibited significantly more apoptotic germ cells than WT mice did after ethanol injection, which was demonstrated by DNA fragmentation, PI staining flow cytometry and TUNEL staining. In addition, histopathological examination revealed that degenerative changes of epithelial component of the tubules occurred in FasL overexpressing transgenic mice while testicular morphology was normal in wild-type mice after acute ethanol exposure, suggesting FasL expression determines the sensitivity of testes to ethanol in mice. In summary, we provide the direct evidences that Fas ligand mediates the apoptosis of testicular germ cells induced by acute ethanol using FasL transgenic mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Enhancement of germ cell apoptosis induced by ethanol in transgenic mice overexpressing Fas Ligand

Jiang

Hua

et al. 2003

Cell Res

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“…7 Numerous studies [8][9][10] have indicated that chronic alcohol abuse in males resulted in decreased testosterone production, reduced sperm output, and testis atrophy. In animals, ethanol exposure of adults can increase germ cell apoptosis 11 and cause an adverse effect on the secretory function of Sertoli cells. 12 Traditionally, palm wine is given to women after childbirth to help stimulate the production of milk as well as to young women in fattening rooms.…”

Section: Introduction Pmentioning

confidence: 99%

Effect of Preservation Methods of Oil Palm Sap (Elaeis guineensis) on the Reproductive Indices of Male Wistar Rats

Ikegwu

Okafor²,

Ochiogu³

2014

Journal of Medicinal Food

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Thirty male Wistar rats, split into five groups of six rats each, were administered different forms of oil palm tree (Elaeis guineensis) sap samples by gavage based on 1.5% of their weekly body weights. Group 1 which served as control received only water, group 2 received pasteurized palm sap (PPS), group 3 received market palm wine (MPW), group 4 received frozen palm sap (FPS), whereas group 5 received fresh palm sap (FrPS). Chemical composition of the sap samples was determined. Normal feed and water were fed ad libitum. After 2 months of treatment, each male rat group was allowed 7 days to mate with six female Wistar rats. Thereafter, blood and epididymal samples were collected for testosterone assay and sperm count, respectively, before they were humanely sacrificed and testicular tissues taken for testicular histology. Litter weight and size of the pups produced by the females of each group were determined at birth. The sap samples contained carbohydrate (0.01-11.71%), protein (1.56-1.95%), ash (0.22-0.35%), moisture (92.55-98.24%), and alcohol (0.26-3.50%). PPS-treated rat group had significantly (P < .05) decreased sperm count (42.60 -23.64 · 10 6 ), abnormal increase in testosterone level, and necrosis in the histology of the testes with reduced spermatogenetic activity, compared with other treatment groups. The female rats crossed with male rats fed on FrPS or FPS produced the highest number of pups followed by the control group. This study demonstrated that the intake of FrPS improved fertility in male animals, but its administration for a long period led to necrotic changes in the testes, whereas pasteurization of palm sap, impacted negatively on the reproductive indices of male animals.

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“…Degeneration of germinal epithelium in rats (Rattus norvegicus) and mice (Mus musculus) in response to hypophysectomy, gonadotrophin and GnRH antibody administration, severe temperature stress, and toxin exposure is associated with increased apoptotic cell death (Tapanainen et al, 1993;Hikim et al, 1995;Shetty et al, 1996;Lee, et al, 1997). Indeed, most studies of testicular apoptosis have examined pathological or supraphysiological states (for example, Franca et al, 2000;Zhu et al, 2000). Seasonal gonadal atrophy represents a natural model for the study of gonadal apoptosis.…”

mentioning

confidence: 99%

Mediation of seasonal testicular regression by apoptosis

Young¹

2001

Reproduction

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Seasonal rhythms in physiology and behaviour are characteristic of most temperate and boreal species (Bronson, 1989). Synchronizing energetically demanding biological functions to the most favourable time of the year enables individuals to cope with recurring stressors such as seasonal declines in food or water availability, or annual fluctuations in ambient temperature. Environmental factors such as food availability, social cues, ambient temperature and the initial predictive cue of daylength (photoperiod) can facilitate or inhibit reproductive function seasonally. These factors maintain testicular function during favourable times of the year in some species (for example, birds), and induce testicular regression or atrophy when environmental conditions are less favourable in others (for example, small mammals). Environmental factors regulate testicular function through the hypothalamic-pituitary-gonadal (HPG) axis. Photoperiod serves as the primary predictive factor in the regulation of reproductive timing in long-and short-day breeding mammals and in most bird species (Wingfield and Kenagy, 1991;Bronson and Heideman, 1994). The general long-day breeding rodent response to seasonal changes in daylength is shown (Fig. 1); however, the actual HPG response to photoperiod is distinct among different species of birds, reptiles and mammals. Supplementary cues such as food and water availability also affect reproductive function directly, serving to fine-tune the initial, general reproductive response to photoperiod (Wingfield and Kenagy, 1991). Environmental factors that stimulate or maintain reproduction promote synthesis and secretion of GnRH from the hypothalamic median eminence, and positively regulate secretion of the gonadotrophins (LH and FSH) from the anterior pituitary (Bronson and Heideman, 1994). In contrast, non-stimulatory environmental factors decrease GnRH (pulse amplitude and frequency) release, resulting in testicular atrophy, reduced spermatogenesis and diminished testosterone production from Leydig cells, the steroidogenic somatic cells in the testicular interstitium (Sinha Hikim and Swerdloff, 1999).During the transition from the breeding to the nonbreeding state, males in most seasonally breeding species undergo 40-90% atrophy in testis mass. Cells must either undergo marked reduction in size, increases in the rate of cell death, or both, to achieve the reduction in volume observed during regression. The rate of cell division may decrease in the testis during regression, indirectly contributing to seasonal atrophy; however, total testicular DNA content in rodents is reduced with non-stimulatory photoperiod exposure, indicating an increase in cell death during regression (Desjardins and Lopez, 1983). Recent studies have examined complex changes that occur in testicular cells during seasonal reproductive regression. In this review, the contribution of apoptosis, or programmed cell death, in the mediation of seasonal atrophy is discussed. Specifically, the review focuses on the interactions of gona...

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Ethanol Exposure Enhances Apoptosis Within the Testes

Abstract: All of these observations suggest that ethanol enhances testicular germ cell apoptosis.

Cited by 69 publications

References 62 publications

Enhancement of germ cell apoptosis induced by ethanol in transgenic mice overexpressing Fas Ligand

Enhancement of germ cell apoptosis induced by ethanol in transgenic mice overexpressing Fas Ligand

Effect of Preservation Methods of Oil Palm Sap (Elaeis guineensis) on the Reproductive Indices of Male Wistar Rats

Mediation of seasonal testicular regression by apoptosis

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