Deoxynivalenol
(DON, vomitoxin) is the most common mycotoxin in
cereals and grains. DON contamination can cause a serious health threat
to humans and farm animals. DON has been reported to exert significant
toxicity effects on the male reproductive system. However, the causes
and mechanisms underlying efforts of DON on sperm and testicular damage
remain largely unclear. In the present study, we thoroughly investigated
this issue. Eighty male BALB/c mice were randomly divided into a control
group (n = 40) and DON treatment group (2.4 mg/kg
of body weight, n = 40). The ratio of testes and
seminal vesicle to body, sperm survival and motility, and morphology
of sperm and testis were observed in DON-treated and control mice.
In addition, the concentrations of reactive oxygen species (ROS) and
malondialdehyde (MDA), the activities of superoxide dismutase (SOD)
and glutathione (GSH), and also the expression levels of JNK/c-Jun
signaling and apoptotic factors such as caspase-3, caspase-8, caspase-9,
Bim, and Bid were analyzed and compared between the two groups. The
results demonstrated that a single topical application of DON significantly
increased the percentage of abnormal sperm and decreased the motility
of sperm, indicating the sperms are damaged by DON. Additionally,
the reduced relative body weight of testis and severe destruction
of testicular morphology were observed. Moreover, the increased levels
of ROS and MDA levels and decreased activities of SOD and GSH were
found in testicular tissues, suggesting that oxidative stress is induced
by DON treatment. Furthermore, DON upregulated the expression of stress-induced
JNK/c-Jun signaling pathway proteins as well as JNK/c-Jun phosphorylation
proteins. In addition, DON could enhance testicular apoptosis by increasing
expression levels of apoptotic genes including Bim, cytochrome c,
caspase 3, caspase 8, and caspase 9. These results suggest that DON
exposure can cause sperm damage, oxidative stress, testicular apoptosis,
and phosphorylation of JNK/c-Jun signaling pathway. The underlying
mechanisms may be that DON induces sperm damage by exacerbating oxidative
stress-mediated testicular apoptosis via JNK/c-Jun signaling pathway.
