Mechanism of cadmium poisoning on testicular injury in mice

Ren, Yanan; Shao, Wenhua; Zuo, Lijun; Zhao, Wei; Qin, Haizhang; Hua, Yingjie; Lu, Dejie; Mi, Chao; Zeng, Su; Zu, Liao

doi:10.3892/ol.2019.10418

Cited by 26 publications

(18 citation statements)

References 40 publications

(41 reference statements)

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“…Hence, besides initiating reproductive toxicity, Cd affects the weight of animals. This finding contradicts some of the data reported in the literature [ 44 , 45 ]. According to Sagba et al [ 46 ], Cd has a negative effect on weight gain.…”

Section: Discussioncontrasting

confidence: 99%

Damage to the Testicular Structure of Rats by Acute Oral Exposure of Cadmium

Iqbal

Cao

Zhao

et al. 2021

IJERPH

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Cadmium (Cd) is one of the most important heavy metal toxicants, used throughout the world at the industrial level. It affects humans through environmental and occupational exposure and animals through the environment. The most severe effects of oral exposure to Cd on the male reproductive system, particularly spermatogenesis, have not been discussed. In this study, we observed the damage to the testes and heritable DNA caused by oral exposure to Cd. Adult male Sprague–Dawley rats were divided into four groups: a control group and three groups treated with 5, 10, and 15 mg Cd/kg/day for 17 days by oral gavage. Our results revealed that Cd significantly decreases weight gain in 10 and 15 mg/kg groups, whereas the 5 mg/kg groups showed no difference in weight gain. The histopathology showed adverse structural effects on the rat testis by significantly reducing the thickness of the tunica albuginea, the diameter of the tubular lumen, and the interstitial space among seminiferous tubules and increasing the height of the epithelium and the diameter of the seminiferous tubules in Cd treated groups. Comet assay in epididymal sperms demonstrated a significant difference in the lengths of the head and comet in all the 3 Cd treated groups, indicating damage in heritable DNA, although variations in daily sperm production were not significant. Only a slight decrease in sperm count was reported in Cd-treated groups as compared to the control group, whereas the tail length, percentage of DNA in head, and tail showed no significant difference in control and all the experimental groups. Overall, our findings indicate that Cd toxicity must be controlled using natural sources, such as herbal medicine or bioremediation, with non-edible plants, because it could considerably affect heritable DNA and induce damage to the reproductive system.

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Section: Discussioncontrasting

confidence: 99%

Damage to the Testicular Structure of Rats by Acute Oral Exposure of Cadmium

Iqbal

Cao

Zhao

et al. 2021

IJERPH

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“…route [ 64 ]. In another experiment, the reduction in the diameter of seminiferous tubules was also found [ 65 ].…”

Section: Cadmium (Cd)mentioning

confidence: 84%

Effects of Cadmium, Lead, and Mercury on the Structure and Function of Reproductive Organs

Massányi

Madeddu

et al. 2020

Toxics

136

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Reproductive organs are essential not only for the life of an individual but also for the survival and development of the species. The response of reproductive organs to toxic substances differs from that of other target organs, and they may serve as an ideal “barometer” for the deleterious effects of environmental pollution on animal and human health. The incidence of infertility, cancers, and associated maladies has increased in the last fifty years or more, while various anthropogenic activities have released into the environment numerous toxic substances, including cadmium, lead, and mercury. Data from epidemiological studies suggested that environmental exposure to cadmium, lead, and mercury may have produced reproductive and developmental toxicity. The present review focused on experimental studies using rats, mice, avian, and rabbits to demonstrate unambiguously effects of cadmium, lead, or mercury on the structure and function of reproductive organs. In addition, relevant human studies are discussed. The experimental studies reviewed have indicated that the testis and ovary are particularly sensitive to cadmium, lead, and mercury because these organs are distinguished by an intense cellular activity, where vital processes of spermatogenesis, oogenesis, and folliculogenesis occur. In ovaries, manifestation of toxicity induced by cadmium, lead, or mercury included decreased follicular growth, occurrence of follicular atresia, degeneration of the corpus luteum, and alterations in cycle. In testes, toxic effects following exposure to cadmium, lead, or mercury included alterations of seminiferous tubules, testicular stroma, and decrease of spermatozoa count, motility and viability, and aberrant spermatozoa morphology.

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“…Sperm is produced by and develops in the testicles, and when the testicles are damaged, it inevitably affects the male's reproductive ability. Cadmium poisoning can aggravate testicular injury and affect the secretion of testosterone, possibly by changing the LHR, 17 alpha-hydroxylase, and eNOS expression levels of testicular stromal cells [28]. Sperm viability can objectively reflect the development of the testis.…”

Section: Discussionmentioning

confidence: 99%

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

Yang

Liu

et al. 2019

Biomolecules

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T-2 toxin is one of the most toxic type A trichothecene mycotoxins in nature, and it exhibits reproductive toxicity. Betulinic acid (BA) is a natural pentacyclic triterpene compound found in species of Betula, and it has been reported to have antioxidant activity. The aim of the present study was to investigate the protective effect of BA on T-2-toxin-induced testicular injury in mice and explore its molecular mechanism. Sixty adult male mice were randomly divided into groups. The mice were pretreated orally with BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and the T-2 toxin (4 mg/kg body weight) was administered via intraperitoneal injection to induce oxidative stress after the last administration of BA. BA pretreatment significantly increased the secreted levels of testosterone and sperm motility. Moreover, BA pretreatment significantly increased the total antioxidant capacity (T-AOC), the activity of SOD and CAT, and the content of GSH, and it reduced the content of MDA. Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax). BA also increased the expression of B-cell lymphoma-2 (Bcl-2). We suggest that BA reduced the oxidative damage induced by T-2 toxin, and that these protective effects may be partially mediated by the JAK2/STAT3 signaling pathway.

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Mechanism of cadmium poisoning on testicular injury in mice

Cited by 26 publications

References 40 publications

Damage to the Testicular Structure of Rats by Acute Oral Exposure of Cadmium

Damage to the Testicular Structure of Rats by Acute Oral Exposure of Cadmium

Effects of Cadmium, Lead, and Mercury on the Structure and Function of Reproductive Organs

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

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