THERE ARE MANY CHEMICALS IN THE FOOD WE EAT EVERY DAY THAT HAVE ESTROGENIC ACTIVITY. THIS TYPE OF ESTROGENS ARE SENTHETIC, NOT NATURAL BUT STILL HAVE ABILITY TO PRODUCE CYSTS AND STERELIZATION. AZOOSPERMIYA AND THE STERILITY IS THE OUTCOME. I read that some companies put DES into meat and ship to third world countries. There are some chemicals that are in plastic bottles and other cane foods. Some companies put chemicals in cows to make them fatter and produce more milk. The milk that you drink after all with all chemicals in it. WE LIVE IN THE WORLD OF TOXINS THAT INTERFERE WITH OUR BODY FUNCTIONS AND PRODUCE DISEASES AND ABNORMALITIES. I suggest eating only organic food without pesticides. Do not drink beverages in plastic bottles. Put in trash everything what is not organic. Brush teeth with toothpaste that does not have fluoride in int. Do not drink tap water. Tap water has estrogenic chemicals in it as well.
To treat epididymal cyst I suggest taking supplements of saw palmetto, vitamin E, golden seal. Will see if it will help to reduce cyst. I have cysts on both testicles for like 10 years already. I hope some day they will shrink.
!!!! HERE IS THE JOURNAL YOU HAVE TO READ TO GET IDEA WHERE CYST COME FROM !!!!!
Journal of Reproduction and Fertility Supplement 53, 247-259
Effects of environmental toxicants on the efferent
ducts, epididymis and fertility
Department of Veterinary Biosciences, College of Veterinary Medicine,
S. Lincoln, University of Illinois, Urbana, IL 61802, USA
Many of the reproductive toxicants have primary effects on the testis, which potentially overshadow effects downstream
on the efferent ducts and epididymis. The specific target of these effects depends upon the dosage and time response. It is
often necessary to design experiments that separate testosterone-dependent responses arising in the testis from direct
effects on epididymal tissues and spermatozoa, to uncover the mechanisms of toxicity in excurrent ducts. Recent studies
have confirmed that chemicals can also alter the time required for sperm transport through the epididymis. Currently there
are approximately twenty chemicals that can be classified as epididymal toxicants. There are fewer toxicants reported for
the efferent ducts, but a few overlap with epididymal effects. The benzimidazole carbamates, like many efferent ductal
toxicants, induce occlusions and subsequent testicular atrophy. The mechanisms appear to be related to fluid reabsorption,
sperm stasis, followed by leukocyte chemotaxis, sperm granulomas, fibrosis and often the formation of abnormal
microcanals. Disruption of oestrogen receptor function in the efferent ducts also interferes with fluid reabsorption and
results in testicular swelling and seminiferous tubular atrophy. Thus, studies in which testicular atrophy occurs after
chronic or subchronic exposures should be examined for lesions in efferent ducts and head of the epididymis. Such lesions
can lead to permanent infertility
Toxicology of the epididymis has received less attention than other regions of the male reproductive system. A search of
the literature for the period 1995-1997 shows that the testis has been the major emphasis in toxicology (nearly 400
papers), while the number of manuscripts focused on toxicity associated with the epididymis is fewer than 90. One problem
has been the difficulty in separating direct versus indirect effects on the excurrent ducts, because altered testicular function
indirectly alters function of the ductal epithelium downstream. The epididymis is dependent upon androgen stimulation;
therefore, any compound that decreases Leydig cell function will decrease androgenic concentration in blood and rete testis
fluid, which will have subsequent effects on the epididymis, sperm maturation and fertility. One complication is the fact
that a primary effect on the testis may become overwhelming and define the long-term effects on fertility~ regardless Of
effects on the epididymis. If there is a decline in spermatogenesis or testicular atrophy ensues, it is of little consequence
that clear cells in the epididymis also disappear. However, it is possible that short-term toxicity targets only the
epididymis or the spermatozoa in transit. For example, (a-chlorohydrin appears to have direct effects on epididymal
spermatozoa without testicular effects, if the dosage is low and exposure time is short (Slott et al., 1997).
If we are to begin separating direct versus indirect effects of toxicants on the male reproductive tract, it is important
that experimental design be given top priority. Examining long-term exposures and moderate to high dosages will often
provide only primary testicular effects that overshadow effects on the epididymis or spermatozoa. In this review, the
ductuli efferentes (efferent ducts) and
C 1998 Journals of Reproduction and Fertitity Ltd
R. A. Hess
Table 1. Pathways for direct effects of toxicants on the epididymis
1. Sperm target
2. Epithelial target
Secretory proteins, ions, etc.
Metabolism, ion flux, organelles
3. Connective tissue target
Blood and lymphatic flow
4. Mixed targets
Indirect action on spermatozoa
epididymis will be considered independently but referred to at times collectively as epididymis. Epididymal toxicants and
their known mechanisms of action will be listed. However, the primary focus will be on a compound that targets the
efferent ducts and seminiferous epithelium. This compound is benomyl, a benzimidazole carbarnate fungicide. We have
studied both this parent compound and its metabolite, carbendazim, because the metabolite is responsible for the primary
effects on male reproduction (Lim and Miller, 1997). An understanding of the short-term, as well as the long-term, effects
is essential if the causes of infertility and testicular atrophy are to be revealed.
Toxicants That Affect the Epididymis
Direct versus indirect effects
The use of two different experimental methods has improved the recognition of effects on epididymal epithelium or
spermatozoa in transit. A good example is cyclophosphamide, which induces lethal mutations in males. Only when short-
term studies were performed or experimental ligation of the efferent ducts was used did the investigators determine direct
effects on epididymal spermatozoa or the epididymal epithelium (Qiu et al., 1995). Methyl chloride is another example of
a toxicant that acts directly on the epididymis (Chellman et al., 1987). However, its mechanism of action is different, as it
works through secondary damage to spermatozoa following an inflammatory response to treatment and the formation of
granulomas. Thus, there are many pathways by which toxicants can affect the epididymis (Table 1) and we have only just
begun to understand these mechanisms in a limited number of chemicals. There are approximately twenty chemicals that
can be classified as epididymal toxicants, either as having direct or indirect effects on the epididymal epithelium or
effects on epididymal spermatozoa (Table 2).
Effects independent of testosterone
Ethane dimethanesulfonate (EDS) and chloroethylmethanesulfonate (CMS) are alkylating antitumour agents that
destroy Leydig cells and thus cause a reduction in testosterone (Klinefelter et al., 1992, 1994a,b). However, both
compounds also produce epididymal lesions. To determine whether the epididymal effects are independent of testicular
effects, Klinefelter et al. (1992, 1994b) used testosterone implants to maintain androgen stimulation of spermatogenesis
and the epididymal epithelium. Both chemicals caused specific disappearance of clear cells in the cauda epididymis,
decreased cauda sperm counts and altered two-dimensional gel patterns of proteins in cauda spermatozoa, all independent
Direct effects o n spermatozoa
TO test-the potential direct effects of EDS on epididymal spermatozoa, Klinefelter et al. (1992) treated spermatozoa
or co-cultured spermatozoa and epididymal epithelium. Using this novel in
Epididymal effects of environmental toxins
Table 2. Effects of toxicants on the epididymis
a b c d e
f g h i j k I
o p q rs
x x x x
Loss of clear cells
x x x
Alter sperm protein
Direct effects on
a, -Chlorohydrin; b, Epichlorohydrin; c, cc-Bromohydrin; d, glycidol (Cooper et al., 1974; Ericsson, 1975; Slott
et al., 1997; Tsang et al., 1981);
e, 6-Chloro-6-deoxyglucose (Tsang et al., 1981; Wong et al., 1980);
f, Cyclophosphamide (Qiu et al., 1995);
g, Methyl chloride (Chellman et al., 1986; Working et al., 1985);
h, Guanethidine (Evans et al., 1972);
i, Ornidizole (Oberlander et al., 1994; Cooper et al., 1997);
j, Methoxychlor (Linder et al., 1992);
k, Anti-androgens (hydroxyflutamide (Klinefelter and Suarez, 1997), cyproterone acetate (Din-Udom et al.,
1985; Tsang et al., 1981), vinclozolin (Kelce et al., 1997));
1, Ethane dimethanesulfonate (Klinefelter et al., 1990; 1994b);
m, Chloroethylmethanesulfonate (Klinefelter et al., 1994a; 1997; Klinefelter and Suarez, 1997);
o, Reserpine (Wen and Wong, 1988);
p, 2,3,7,8-Tetrachlorodibenzo-p-dioxin (Cray et al., 1997);
q, 2,3-Dihydro-2-1-naphthyl -41H-quinazolinone (Ericsson, 1971);
r, PCB169 (Gray et al., 1995);
s, Cadmium (Nagy, 1985).
2 See also review by Klinefelter and Hess (1998).
vitro method, they found that the effects of EDS on spermatozoa were mediated through the epididymal-epithelium and not
directly on the spermatozoa. There are other examples of toxicants having direct effects on spermatozoa within the
epididymal lumen. However, these effects are dose dependent; direct effects on spermatozoa occur only at the lower
dosages, while higher doses of the
R. A. Hess
same chemical can cause many pathological changes in the epididymis. In this category, a-chlorohydrin is the best
example. At lower dosages, dose-dependent effects on sperm velocity and fertility were significant in the absence of
epididymal granulomas (Slott et al., 1997), possibly mediated by the inhibition of glycolysis in the spermatozoa.
Spermatocoeles and granulomas are typical responses in both efferent ducts and the caput epididymis after treatments at
higher dosages (Cooper et al., 1974).
Alterations in sperm transit time
Another mechanism by which chemicals may interfere with fertility is an alteration in sperm transit time through the
epididymis. Oestrogen treatment accelerates the rate of sperm transport in the epididymis (Meistrich et al., 1975). Other
experiments have also demonstrated that sperm transport can be altered by disruption of sympathetic or adrenergic
innervation of the epididymis (Evans et al-, 1972), and thereby alter ion flux, particularly Cl- secretion (Wen and Wong,
1988; Wong, 1990). More recent studies have shown that chloroethyl-methanesulphonate and hydroxyflutamide accelerate
sperm transit through the epididymis (Klinefelter and Suarez, 1997), supporting the findings that castration or cyproterone
acetate treatment enhance sperm transport. Interestingly, in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin also
results in altered sperm transport without obvious testicular effects in adult life (Gray et al., 1997). In the light of these
studies, future efforts should be devoted to uncover the physiological mechanisms responsible for sperm transport that are
the target of exposure to environmental chemicals.
Toxicants That Affect Efferent Ducts
Reports indicate that smoking and ten reported compounds induce some type of toxic response in the efferent ducts (Table
3). Unfortunately, a clear understanding of their mechanisms of toxicity is lacking. However, for some chemicals there are
biochemical data suggesting routes of induced injury. For example, a-chlorohydrin (or a metabolite) and 6-chloro-6-
deoxyglucose (CDG) cause reductions in glucose transport and glucose metabolism (Hinton et al., 1983), which could
indirectly interfere with energy-dependent processes such as ion transport, in addition to their direct effects on
spermatozoa. It is interesting that a-chlorohydrin and epi-chlorohydrin are metabolites of 1,2-dibromo-3chloropropane
(DBCP), a chemical responsible for the first well known case of infertility in humans caused by chemical exposure
(Whorton et al., 1979). All three compounds cause kidney dysfunction as well as epididymal lesions (Kluwe et al., 1983).
Although the literature does not indicate that DBCP affects the efferent ducts, Kluwe et al. (1983) did report 'dilatation of
the seminiferous tubules' and long-term tubular atrophy, which are common responses to occlusion of these ducts and seen
following exposure to a-chlorohydrin and epichlorohydrin (Cooper and Jackson, 1972; Cooper and Jackson, 1973; Jones,
1978; KIuwe et al., 1983). Thus, it appears that the general mechanism of toxicity for these chemicals is an alteration of
fluid reabsorption followed by sperm stasis and ductal occlusion. In general, there are at least six major responses of the
efferent ducts to environmental toxins, which can lead to reduced fertility and even testicular atrophy (Table 4).
An examination of the chemicals listed in Table 3 indicates that many toxicants of the efferent ducts induce occlusions.
This would suggest an interference with fluid reabsorption, or that other factors such as granulomas or inflammation cause
the luminal fluid to become stagnant. In 1943, Wakeley stated that most epididymal cysts in man arise from dysfunction of
the efferent ducts. As more chemical toxicants are examined, this early prediction appears to be correct for animal models,
too. Several mechanisms could be involved in the pathophysiology of ductal occlusions. One possibility is direct or
indirect disruption of Cl- secretions, which appear to be important for normal flow of spermatozoa in the proximal
epididymis (Chan et al., 1995). mRNA encoding cystic fibrosis
Epididymal effects of environmental toxins
Table 3. Effects of toxicants on the efferent ducts
I a, Benomyl@ (Hess et al., 1991);
b, Carbendazim (Carter et al., 1987; Gray et al., 1990; Nakai et al., 1992; Nakai et al., 1993; Rehnberg et al.,
c, a- and epi-Chlorohydrin (Cooper et al., 1974; Ford and Wailes, 1981; Hoffer et al., 1975; Jones 1978);
d, Ethylenedimethane sulfonate (Cooper and Jackson, 1972; Cooper and Jackson, 1973);
e, 6-Chloro-6-deoxyglucose (Ford and Waites, 1981);
f, Quinazolinone (Ericsson, 1975);
g, 1,3-Dinitrobenzene (Linder et al., 1988a);
h, Uranyl nitrate (Mason and Young, 1967);
i, Glycidol (Jones and O'Brien, 1980);
j, Cadmium (Nagy, 1985);
k, Fluoride (Susheela and Kumar, 1991).
2 See also reviews by Ilio and Hess, 1994; and Klinefelter and Hess, 1998.
transmembrane conductance regulator (CFTR) is more prevalent in the proximal regions of the male tract (Trezise et al., 1993) and adult
cystic fibrosis patients are infertile, often due to epididymal obstruction (Gaillard et al., 1997).
Effects of Benzimidazole Carbarnate Fungicides on Efferent Ducts and Fertility
Effects on fertility
Benomyl (methyl 1-(butylcarbamoyl)-2-benzimidazole carbarnate) and its metabolite carbendazim (methyl 2-benzimidazole carbarnate)
are both highly effective fungicides and nematocides. Their fungicidal action is due to their ability to disrupt microtubule formation, an effect
that is also extended to mammalian cells (see Hess et al., 1991). Regulation of these chemicals by the US Environmental Protection Agency
was based partially on their reproductive toxicity, which is associated with testicular degeneration (Carter and Laskey, 1982) and decreased
fertility (Carter et al., 1987; Gray et al., 1990; Linder et al., 1988b; Torchinskiy et al., 1976). However, the early studies of
benzimidazole compounds did not establish mechanisms of testicular atrophy. Infertility occurred in 50% of the males after the first week of
exposure to a single dose of carbendazim (400 mg kg-1), but histopathological examination of the testes revealed large variation in tubular
atrophy (Carter, 1987). At first, atrophy was assumed to be the result of action of carbendazim as a microtubule poison, which has been
shown subsequently to cause necrosis of mitotic and meiotic cells in the testis (Nakai and Hess, 1997) and the formation of abnormal
spermatids (Nakai et al., 1997). Other workers found effects on hormones in serum and testicular fluids and attempted to relate the long-term
effects on sperm production to an inhibition of the testicular
R. A. Hess
Table 4. Major responses of the efferent ductules to environmental toxins and
Associated toxicants or
Increased reabsorption of Benomyl'; carbendazim2
Increased sperm concentration/
Decreased sperm concentration/
of luminal fluid
dilution/ luminal dilation
Epithelial desquamation a-chlorohydrin3
Benomyl'; carbendazim2; Testicular atrophy
Benomyl'; carbendazim2; Decreased fertility
'(Hess et al., 1991).
2 (Nakai et al., 1992).
'(Hoffer et al., 1975).
'(Linder et al., 1988).
hypothalamus-pituitary feedback loop (Goldman et al., 1989; Rehnberg et al., 1989). However, upon further examination
of the histopathology, it was found that two sequential events, first in the testis and then in the efferent ducts, could
answer many of the questions regarding hormonal changes, long-term atrophy of seminiferous tubules and why some males
became irreversibly infertile.
Effects on seminiferous epithelium
Benzimidazole carbarnate compounds cause premature sloughing of germ cells along with cleaved processes of Sertoli
cell cytoplasm (Hess et al., 1991; Nakai and Hess, 1994), necrosis of mitotic spermatogonia and meiotic spermatocytes
(Nakai and Hess, 1997) and seminiferous tubular atrophy (Carter et al., 1987; Hess et al., 1991; Nakai et al., 1992). The
proposed mechanism contributing to sloughing is deformation of Sertoli cell cytoplasm due to the disruption of
microtubules (Nakai and Hess, 1994; Nakai et al., 1995). Recovery from massive sloughing of germ cells is possible if the
efferent ducts remain intact; however, abnormal spermatids are formed several days after a single exposure to carbendazim
and may affect fertility long after the initial testicular injury (Nakai et al., 1997). These effects occur in testes with intact
efferent ducts. Therefore, carbendazim can have direct effects on the seminiferous epithelium at lower dosages, independent
of efferent duct dysfunction. On the basis of the severity of germ cell sloughing, we first hypothesized that occlusions in
efferent ducts were caused by cellular debris that clogged the lumen only at ductal junctions. However, other chemicals also
induce massive sloughing of germ cells without efferent ductal occlusions; therefore, an alternative explanation was
Effects on efferent ducts
Occlusion of the efferent ducts (Fig. 1) is common after exposure to the fungicide benomyl or its metabolite
carbendazim (Hess et al., 1991; Nakai et al., 1992). This response is rapid, as an increase in testis weight is detected as
early as 8 h after exposure (Nakai et al., 1992). A single dose appears to be sufficient to induce ductal occlusions, but a
comparison of 70 day, single-exposure data (Nakai et al.,
Epididymal effects of environmental toxins
Fig. 1. (a) A drawing of microdissected efferent ducts collected from a rat 48 h after treatment
with a single dose of carbendazim (400 mg kg-1). This type of data was collected from
photographs (similar to (b)) and tabulated in Table 5. Occlusions are noted as thick dark areas
(arrows) near the rete testis. Ductal regions are identified as proximal, conus and terminus. The
terminus is a single ductule that joins the initial segment epididymidis (Is), and in this case
contained a small blind ending tubule (131). (b) A photograph of microdissected efferent ducts
showing occlusions (arrows). A region of normal size is noted by an asterisk near a junction.
Scale bar represents 1 mm.
1992) with 245 days following exposure for 10 days (Carter et al., 1987) is noteworthy because the percentage of
testes with 'total seminiferous tubular atrophy' was 21% on day 70 and 50% on day 245. This suggests that either
seminiferous tubular regression continues long after treatment has stopped or that the additional doses were
effective in spreading damage to a greater number of efferent ducts.
Microdissection of occluded efferent ducts was performed to determine specific locations of the
benzimidazole lesions (Table 5). At 12 h after treatment 75.8% of the ductules were occluded and by 24 h nearly
85% were occluded. Overall, 56% of the occlusions were located in the initial zone, 15% at junctions and 44% in
the conus vasculosa. No occlusions were observed in the common efferent duct. Further measurements confirmed
that the initial zone was the primary site of occlusions, as the ductules in this zone were significantly longer (41.9
mm) in treated animals compared with controls (30.7 mm). The length of the common duct did not change: 19.6
mm and 18.1 mm. in control and treated, rcspectively.
After occlusions were formed in the efferent ducts, an inflammatory response was initiated, approximately 2-
4 h later. The severity of response was dose dependent, but the onset of occlusion
and time to first appearance of neutrophils in the connective tissue remained the same regardless of dosage. In
controls, occlusions were not present and neutrophilic leukocytes were absent. However, 2 h after treatment,
exfoliated spermatids were present in the lumen of the efferent ducts and most ductules were engorged by 4 h.
Complete occlusion of the ductules occurred at 6-8 h, before the infiltration of neutrophils, which corresponded to
a build-up of fluid in the testis and increased testis weight (Nakai et al., 1992). Neutrophils began to appear in the
connective tissue between 8-12 h after
Table 5. Carbendazim-induced occlusions of the ductuli efferentes in the adult rat'
Time (h) Number Number
Location of occlusions'
treatment animals ductules occluded occluded' Proximal junction Conus Terminus
1 400 mg kg-' by single oral gavage.
2 Overall, 80.1% of the ductules were occluded.
3 Overall, occlusions in the proximal ductule (56%); at junctions (15%); in the conus (44%); in the
treatment; therefore, it is concluded that benzimidazole carbamates have direct effects on
efferent ducts rather than an indirect reaction following inflammation.
The neutrophils migrated between the junctions of endothelial cells lining small venules, producing
limited haemorrhage into the connective tissue. As the leukocytes migrated between the thin smooth
muscle layers of the efferent ducts, some of the muscle cells were destroyed. By 48 h, neutrophils formed
between 2-5 solid layers of cells around the base of the ductules (Fig. 2a,b), where they eroded the basal
lamina before penetrating between epithelial cells. Neutrophils then phagocytosed luminal debris and
caused luminal contents to erupt into the lamina propria. Thus, neutrophils exhibited a specific
chernotactic response toward efferent ducts containing stagnant spermatozoa and exfoliated spermatids.
The leukocytes attempted to seal off the luminal contents but appeared to damage the epithelium in the
process, which may have contributed to subsequent formation of fibrotic lesions and permanent
The response of efferent ductal epithelium to injury induced by occlusions appears to be dependent
upon the degree of inflammation caused by the trauma. An acute inflammatory reaction may be induced
by the compacted luminal contents, causing the ductal lumen to dilate (Fig. 2c). It is likely that the
ductal epithelium, stretched excessively by a large bolus of testicular debris, releases a chernotactic
substance, possibly a cytokine of the interleukin superfamily, which then recruits large numbers of
neutrophils. Leakage of sperm antigens may draw the neutrophils toward the lumen and stimulate
phagocytic activity. In other organ systems, indirect damage caused by neutrophil emigration into the
interstitium and through the epithelium promotes granuloma formation and fibroblast activity (see
review by Nakai et al., 1993). Thus, fibrotic lesions may be an indirect result of neutrophil damage
rather than direct effects of epithelial injury.
Epithelia with medium inflammatory responses often exhibited irregular epithelial growth along the
edge of luminal contents and formed multiple abnormal ductules (Fig. 2d). These abnormal ductules,
formed by the migration of the original epithelia and growth at the periphery of the occluded lumen,
indicated that recanalization was attempted by 16 days after treatment (Nakai et al., 1993). Epithelial
cells of the microcanals were similar in appearance to those of blind ending tubules (Guttroff et al.,
1992). No evidence was found to indicate that microcanals formed patent connections between rete
Efferent ducts respond to toxic insult by at least two different means (Fig. 3): an increased rate of fluid
reabsorption or decreased secretions (i.e. Cl-) ; or a decreased rate of reabsorption or increased
secretions. The first response leads to increased viscosity of luminal fluids, sperm stasis, ductal
occlusions, granulomas and possibly fibrosis. The second response dilutes the luminal fluid, decreases
sperm concentration, and leads to a decrease in sperm transit time through the epididymis. The
mechanism by which benzimidazole chemicals disrupt fluid reabsorption is not
Epididymal effects of environmental toxins
Fig. 2. (a) Efferent ducts from a control rat showing the normal diameter (Ed; bar) in the proximal
conus region. (b) Occluded efferent ductule from a rat treated with a single dose of carbendazim (400
mg kg 1) and fixed by vascular perfusion 48 h after treatment. The lumen is occluded with sloughed
debris (SI) from the testis. The epithelium (E) is disorganized and shows evidence of sperm
phagocytosis. Neutrophilic leukocytes (arrows) completely surround the basement membrane. (c)
A single occluded efferent ductule 48 h after treatment with carbendazim (400 mg kg-1). The lumen is
filled with debris and the diameter (Ed; bar) of the ductule has nearly doubled in size. Neutrophils
line the basement membrane and are found in the lumen (dark staining nuclei). (d) Occluded efferent
ducts 70 days after treatment with carbendazim (400 mg kg-1) show both the fibrotic lesions (F) and
known. We have limited data showing a dose-dependent increase in the activity of Na+,K+-ATPase
(Table 6), which may result from the disruption of cytoskeletal elements (Jordan et al., 1995). However,
effects on other pathways, such as Cl secretion, should also be considered. Regardless of mechanisms or
the toxicant involved, once ductules become blocked, long-term results are the same, as testicular
atrophy and infertility are produced. Accordingly, long-term testicular atrophy after subchronic and
acute multiple exposure to any toxicant could be explained by potential efferent ductal dysfunction, a
hypothesis that should be examined routinely by histopathology.
Cessation of fluid reabsorption, as seen in the oestrogen receptor knockout mouse, also leads to
fluid build up within the testis and subsequent seminiferous tubular atrophy (Hess et al., 1997). Thus, it
appears that oestrogen may be required for normal fertility in the male. At least in the mouse, oestrogen
receptor-cc is required. This new role for oestrogens in the male reproductive tract raises renewed interest
in the effects of xenoestrogens or environmental oestrogenic chemicals on male fertility and the decline
in sperm counts. Are these effects due only to developmental anomalies, as first hypothesized (Sharpe
and Skakkebaek, 1993)? Or is it possible that exposure of adults also produces oligospermia or a decline
in sperm counts by the dilution of caput spermatozoa due to the inability to reabsorb fluid properly in
efferent ducts (Hess et al., 1997)? Increases in
R. A. Hess
Table 6. The effect of carbendazim on N+,K+-ATPase activity in the the ductuli
efferentes of adult rats'
pmol p-nitrophenol mm-' tubule-' h
7143 ą 320,
7767 ą 540ab
Single exposure by oral gavage. For details of methods, see Ilio and Hess
(1992). Significant differences are indicated by different superscripts (P <
Fig. 3. (a) An illustration of toxicant effects that lead to an excessive amount of fluid reabsorption leaving behind a
higher concentration of spermatozoa, protein and cellular debris in the lumen. The consequences of this effect are
similar to those seen following exposure to carbendazim and lead to increases in the viscosity of luminal contents, sperm
stasis, occlusions, granulomas and fibrosis. (b) An illustration of an effect leading to decreased reabsorption or
increased secretions of Cl- into the lumen. The consequences of this response are similar to those observed in the
oestrogen receptor knockout mouse (Hess et al., 1997), which lead to increased dilution of semen, increased luminal
diameter, and decreases in sperm concentration and possibly sperm transit time.
Epididymal effects of environmental toxins
abnormal sperm morphology could also result from abnormal fluid reabsorption, as normal spermatozoa
leaving the testis would fail to mature in the epididymis if the surrounding luminal fluid did not contain
the necessary concentration of factors required for sperm maturation. Thus, efferent duct dysfunction can
interfere with fertility through several mechanisms and environmental chemicals have the potential to
cause these effects. Future studies must address not only the pathophysiological mechanisms leading to
testicular atrophy, but also the biochemical and molecular mechanisms associated with the regulation of
ion and water flux across the ductal epithelium and their relationship to male infertility.
I had a spermatocele that grew to the size of a smaller orange. I also discovered that my testosterone levels were low. My doctor, not with any connection between the two in mind, put me on a Testosterone supplementation plan - 200mg every other week.
From the time I started getting the Testosterone shots, my spermatocele has dramatically shrunk. It is now about the size of a Robin's Egg.
Color me stunned.
I have had a spermatocele over my left testicle since 2008. It was about the size of Milk Dud when I found it. Now in 2017 it's the size of a clementine orange. It is extremely uncomfortable now. The immense size of the thing has atrophied both testicles to less than half the size they used to be. Sexual intercourse is starting to become more difficult and potentially painful especially my when wife is on top. I have also had trouble maintaining an erection as well. Thank god for Viagra.
I have a theory on how the spermatocele came into existence. In 2007 I was taking part in an hour long spin class. The seats on these machines were horribly uncomfortable. There was a long set where we were sitting down while peddling, like fifteen minutes. After that class my whole scrotum went numb for two weeks. So I'm wondering if whatever injury created that numbness also created this titanic spermatocele. It was probably six months before it became large enough to be noticed.
I also have a partial theory about how the thing grew to it's gargantuan size. Sometimes when I would masturbate, at the moment of climax I would squeeze my urethra shut to avoid making a mess all over. So now I'm wondering since the spermatocele was already there if holding the semen in instead of releasing it might have caused more fluids to be added to the cyst. Of course my theory could be wrong. I'm not sure how everything is connected and how fluidly everything transfers from each piece of the anatomy to the next, but something caused this monstrosity. And it's starting to piss me off now. I was originally going to have the thing surgically removed back in February until I saw the procedure on YouTube. The surgeon makes a rather large incision across the scrotum. The incision has to be large enough to expel the spermatocele and both testicles, so in my case huge.. Then they cut the fibers and capillaries around the cele. This is when I rejected the surgical option. I have read several internet postings from men who have gone this route and regretted it.
For one, they were in extreme pain for over a week. The actual scrotum is not designed to be sewn all together, it sort of has several layers independent of each other. One guy's incision started to rupture, needing more surgery. All of them mentioned that their scrotums became permanently numb by the nerve damage from the incision. I personally cannot deal with having a numbed scrotum again, especially permanently. Additionally, the after effects of the actual surgery itself can cause new spermatoceles to genesis.
The ultra sound I had last year told me that there are five tiny spermatoceles next to the big one. So any one of them could someday sprout like the cue ball sized one it have now. What I can say now is the spermatocele has started to out live the tolerance I've given it all this time. I've started to feel testicle pain on occasion. It feels just like a kick in the balls that doesn't stop for an hour. I am trying to find a doctor who would perform an aspiration on the thing to at least get it down to half the size or less. Of course there's a chance of the thing refilling itself, but that beats permanent numbness. There is also a sclerotherapy procedure which is a partial aspiration with the injection of a chemical that irritates the entrance of the spermatocele causing it to scar closed, cutting off the flow of new spermatic fluids. I also have acquired some hyperdemic needles to perform a self aspiration if I need to. I'm currently scouring the internet for knowledge on how to safely perform procedure this on myself.