Chronic alcohol administration causes expression of calprotectin and RAGE altering the distribution of zinc ions in mouse testis
Open accessAbstract
Several studies reported that chronic alcohol consumption alters the intestinal mucosa barrier, and subsequent entrance of endotoxins into the bloodstream. In many tissues endotoxin exposure causes the expression of calprotectin (CP) and the receptor for advanced glycation -end products (RAGE). In this study we investigated whether chronic alcohol administration causes expression of CP and RAGE in mouse testis. The distribution of free and loosely bound Zn(2+) (FLB-Zn(2+)) in the testicular tissues was also evaluated. Alcohol-induced testicular damage was documented by measuring testosterone blood levels and by light and electron microscope studies. Twenty mice were treated daily for three weeks with 3.0 g/kg of a 25% solution of alcohol. Ten mice were treated in the same period of time with a solution of maltose dextrins, isocaloric to alcohol. Twenty untreated mice were used as controls. Alcohol treated mice showed diffuse expression of CP and RAGE in the interstitial cells. RAGE was found also in the basal compartment of the seminiferous tubules. Depletion of FLB-Zn(2+) was observed in the adluminal compartment of the seminiferous tubules. Expression of CP and RAGE was not found in control mice and maltose dextrin treated mice. Our results indicated novel mechanisms by which alcohol acts in testis. Indeed, CP and RAGE may cause the generation of oxidants and inflammatory mediators, with negative impact on testicular functions. Depletion of FLB-Zn(2+) may contribute to the dysregulation of spermatogenesis.
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Excessive alcohol consumption is known to cause testis dysfunction and degeneration, possibly by increasing oxidative stress; alcohol intake can induce RAGE overexpression in the testis, and prolonged ethanol exposure stimulates RAGE activation to produce oxidative stress and inflammatory mediators, leading to testicular dysfunction and degeneration.
“Excessive alcohol consumption is known to cause testis dysfunction and degeneration, possibly by increasing oxidative stress.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [259]
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- Authors
- Giannessi, F., Scavuzzo, M. C., Giambelluca, M. A., Fornai, F., Morelli, G., & Ruffoli, R.
- Affiliations
- University of Pisa (IT)
- Corresponding author
- Giannessi, Francesco
- Venue
- Systems Biology in Reproductive Medicine
- Publisher
- Informa UK Limited
- Published
- 2014-08-20
- Volume
- 61
- Issue
- 1
- Pages
- 18-25
- ISSN
- 1939-6368 (ISSN-L)
- 1939-6376
- OpenAlex
- W1990160513
- Cited by
- 3
- References
- 44
- Citations by year
- 2023: 1 · 2022: 1 · 2021: 1
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Systems Biology in Reproductive Medicine (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- chronic alcohol administration, calprotectin, receptor for advanced glycation end products, zinc distribution, testis, seminiferous tubules, testosterone, spermatogenesis, oxidative stress, inflammation, endotoxemia
- MeSH terms
- Receptor for Advanced Glycation End Products, Ethanol, Animals, Male, Receptors, Immunologic, Testis, Zinc, Leukocyte L1 Antigen Complex, Mice
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