Mammalian Epididymis Antioxidant Equipment

Before going into the specific tools with which the epididymis protects spermatozoa from oxidative insults, it should be noted that the characteristic anatomical features of this tissue favor low oxidative stress. In particular, the scrotal position of the

Mammalian epididymis antioxydant strategies and equipment.

General context

°low temperature (scrotal position)

Reduced oxidative stress

°low oxygen tension (low blood supply)

Specific actors

°Non-enzymatic primary antioxidants

* Gluthathione (GSH)

* Thiol-containing compounds

* Ascorbic acid / uric acid

* L-carnitine / acetyl-L-carnitine

* Taurine / Hypotaurine

* Clusterin

* Albumin / Lactoferrin

"Enzymatic primary antioxidants

* Superoxide dismutase (SOD)

* Glutathione peroxidases (GPx)

* Catalase (CAT)

* Indoleamine dioxygenase (IDO)

* Peroxiredoxins (PRDX)

* Glutathione S transferase (GST)

Fig. 5.1 Diagrammatic representation of the major antioxidant strategies used by the mammalian epididymis to cope with oxidative stress

Fig. 5.1 Diagrammatic representation of the major antioxidant strategies used by the mammalian epididymis to cope with oxidative stress epididymis helps maintain a temperature about 2-3°C below body temperature. In addition, blood supply to the tail of the epididymis corresponding to the storage part of the organ is reduced, giving a low oxygen tension (PO2). Both low epididy-mal temperature and low PO2 contribute to reduced oxidative stress on the spermatozoa and consequently enhanced sperm survival (Fig. 5.1).

To maintain a proper balance between ROS' beneficial and detrimental actions around epididymal transiting spermatozoa, the luminal compartment of the mammalian epididymis possesses several tools acting in combination (Fig. 5.1). As in all tissues, cells, and/or biological fluids, ROS are disposed of in the mammalian epididymis by both nonenzymatic and enzymatic players grouped under the name of primary antioxidants. It appears that the mammalian epididymis relies more on enzymatic antioxidant scavengers to protect transiting spermatozoa against ROSmediated insults efficiently than on nonenzymatic scavengers. This is supported by two observations: first, the mammalian epididymis was shown to express a large variety of antioxidant enzymes, some of them being unique to this tissue [6-8]. Second, it was recently shown with a transgenic mouse model that, when the major epididymal luminal scavenging enzyme is absent, spermatozoa readily suffer oxida-tive injury [9]. These observations support the idea, at least in mouse, that nonenzy-matic scavengers present in the luminal fluid are not sufficient to compensate efficiently for the loss of enzymatic antioxidant protection.

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