Kim, Il-Hwan;Kim, Yong-Bum;Son, Hwa-Young;Cho, Sung-Whan;Ha, Chang-Su;Kang, Boo-Hyon
Proceedings of the Korean Society of Toxicology Conference
/
2002.05a
/
pp.96-96
/
2002
Zearalenone (ZEA), a nonsteroidal estrogenic mycotoxin, is known to cause toxicity of testis in male rats. To investigate whether apoptosis is involved in ZEA-induced testicular toxicity and to identify the stage and target germ cell type, 10-weeks-old Sprague-Dawley male rats were treated with a single intraperitoneal (i.p.) dose of ZEA (5mg/kg) and euthanized at 3, 6, 12, 24, and 48 h subsequently.(omitted)
Objective: Oxidative stress has been suggested as a possible mechanism for the adverse effects of heavy metal toxicity on male reproduction. Cichorium intybus L. is used in Iranian folk medicine as a hepatoprotective agent as well as for its supposed fertility-enhancing properties. The present study was performed to investigate whether the ethanolic extract of C. intybus leaves could protect male rats against lead-induced testicular oxidative stress. Methods: In this experimental study, adult Wistar rats were treated with 0.1% lead acetate in drinking water alone or with 50, 100, or 200 mg/kg body weight of C. intybus extract via gavage once daily for 70 days. The weight of their reproductive organs, levels of serum hormones, histometric parameters of the seminiferous tubules, epidydimal sperm quality, and oxidative stress status were evaluated. Results: The testis weight, seminiferous tubule diameter, epididymal sperm count, serum testosterone level, and testicular levels of superoxide dismutase and glutathione peroxidase were significantly reduced (p< 0.05) in the lead-treated rats. Moreover, significantly (p< 0.05) higher levels of malondialdehyde were observed in the lead-exposed group compared to the control. However, the co-administration of C. intybus ethanolic extract in lead-treated rats was associated with a significant improvement in reproductive parameters. Conclusion: We conclude that C. intybus leaf extract has the potential to prevent lead-induced testicular toxicity and to suppress the adverse effects of lead on male reproductive health.
Journal of the Korean Society of Food Science and Nutrition
/
v.34
no.8
/
pp.1169-1174
/
2005
This study was carried out to investigate the biological effect of deer's antler velvet on the testicular toxicity of rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD ). Thirty male rats were divided into three equal groups. The control group received vehicle (DMSO/acetone/soybean oil mixture) and saline; single dose of 50 $/mu$g/kg body weight TCDD was injected intraperitoneally into the single TCDD-treated and test group. Test group received ethanol extract of antler velvet (EAV) at daily dose of 20 mg/kg body weight for 5 weeks from one week before TCDD exposure. Decrease in body weight increment was less remarkable in test group compared with that of TCDD-treated group. TCDD-induced decrease in testicular weight, microtubular diameter and Johnson's score, and lesion were significantly alleviated by the treatment of EAV. This result led us to the conclusion that antler velvet can attenuate TCDD-induced testicular toxicity in rats.
This study was carried out to evaluate the testicular toxicity of 2-bromopropane (2-BP), which recently caused occupational intoxication on the reproductive and hematopoietic system in Koreans, using light microscopy, immunohistochemistry and flow cytometry. 10 weeks old male Sprague-Dawley (SD) rats were treated with 0.5 g/㎏/day of 2-BP orally for 8 consecutive weeks. The testes of the rats were vascularly perfused with Karnovsky's solution or immersed in Bouin's solution, embedded in plastic and evaluated with light microscopy. And relative proportions of haploid, diploid, and tetra-ploid states of DNA ploidy in the testicular cell suspensions of the SD rats were examined by flow cytometry. 2-BP induced severe testicular atrophy, depletion and degeneration of spermatogonia, spermatocytes, and spermatids and mild hyperplasia of Leydig cells without significant morphological changes. The Leydig cell hyperplasia was confirmed by immunohistochemistry using proliferating cell nuclear antigen (PCNA). The immunopositive cells against PCNA were observed in the nuclei oj some interstitial cells. Relative proportions of haploid states of DNA ploidy decreased in the atrophic testicular cell suspensions comparing with those of the control. In conclusion, 2-BP induced testicular atrophy with Leydig cell hyperplasia as examined by histopathology, immunohistochemistry and DNA flow cytometry.
Cadmium (Cd) is known to exert gonadotoxic and spermiotoxic effects. The present study was performed to investigate the morphological effects and metallothionein (MT) expression by zinc pretreatment in the course of time of cadmium-induced testicular injury in rat. Fifty male Spraque-Dawley rats weighing 160~180 g were divided into two groups : saline-pretreated cadmium group and zinc-pretreated cadmium group. Rats of two groups received subcutaneous injection of saline and 100 mg/kg $ZnSO_4$ at 0, 2, 5 and 8 hrs intervals respectively. Cadmium chloride (4.5 mg/kg $CdCl_2$) was administrated intraperitoneally at 2 hrs after zinc injection and rats were killed 0, 12, 24, 48 and 72 hrs later. Testicular tissue damages, interstitial (Leydig) cells status and MT expression were determined using hematoxylin-eosin stained sections and a computerized image analysis system on sections immunostained with a mouse anti-metallothionein respectively. Zinc pretreatment was significantly reduced testicular damages in five pathological categories after cadmium administation. The number of surviving interstitial cells was significantly higher in the zinc-pretreated group than in the saline-preatreated group at 48 and 72 hrs after cadmium administration. Non-damaged testis showed the positivity of MT staining in spermatogenic cells, Sertoli cells and endothelium of blood vessel, but not in the Leydig cells. The positivity of MT staining in saline-pretreated group was significantly reduced at 24 hrs after cadmium administration, whereas zinc-pretreated group showed strong MT positive staining similar to the 0 hr by 42 hrs after cadmium administration. In damaged testis, MT positive staining was also observed in the Leydig cells of both groups. These results suggest that a major preventive effect of zinc against cadmium-induced testicular toxicity may be due to its ability to reduce the cytotoxicity of cadmium in spermatogenic cells and Leydig cells by inhibiting the susceptibility of the testis to cadmium but not MT production by cadmium.
Cadmium (Cd) is known to exert gonadotoxic and spermiotoxic effects. The present study was performed to investigate the morphological effects and metallothionein (MT) expression by zinc pretreatment in the course of time of cadmium-induced testicular injury in rat. Fifty male Spraque-Dawley rats weighing 160-180 g were divided into two groups: saline-pretreated cadmium group and zinc-pretreated cadmium group. Rats of two groups received subcutaneous injection of saline and 100 mg/kg $ZnSO_4$ at 0, 2, 5 and 8 hrs intervals respectively. Cadmium chloride (4.5 mg/kg $CdCl_2$) was administrated intraperitoneally at 2 hr after zinc injection and rats were killed 0, 12, 24, 48 and 72 hrs later. Testicular tissue damages, Interstitial (Leydig) cells status and MT expression were determined using hematoxylin-eosin stained sections and a computerized image analysis system on sections immunostained with a mouse anti-metallothionein respectively. Zinc pretreatment was significantly reduced testicular damages in five pathological categories after cadmium administation. The number of surviving interstitial cells was significantly higher in the zinc-pretreated group than in the saline-preatreated group at 48 and 72 hrs after cadmium administration. Non-damaged testis showed the positivity of MT staining in spermatogenic cells, Sertoli cells and endothelium of blood vessel, but not in the Leydig cells. The potitivity of MT staining in saline-pretreated group was significantly reduced at 24 hrs after cadmium administration, whereas zinc-pretreated group showed strong MT positive staining similar to the 0 hr by 42 hrs after cadmium administration. In damaged testis, MT positive staining was also observed in the Leydig cells of both groups. These results suggest a major preventive effect of zinc against cadmium-induced testiculat toxicity may be due to its ability to reduce the cytotoxicity of cadmium in spermatogenic cells and Leydig cells by inhibiting the susceptibility of the testis to cadmium but not MT production by cadmium.
The toxicity of DA-125. a new anthracycline anticancer agent, on the male reproductive system was studied in Sprague-Dawley rats. Forty male rats were rando$m\ell$y assigned to Jour groups with ten rats in each group and given single intraveneous doses of DA-125 at dose levels of 0. 12.5. 25. and 50 mg/kg body weight. On day 56 after treatment the animals were allowed to mate. and their male reproductive Junctions and organs were examined in detail. Copulated females were sacrificed on day 20 of gestation for examination of embryo-fetal development. One out of ten rats in the 50 mg/kg group died on day 12 after treatment. Clinical signs such as emaciation. sedation, anorexia. swelling. dark material around eye. alopecia. and diarrhea were observed in the 25 and/or 50 mg/kg groups. Reduction in the body weight gain. decrease in the absolute weights of testes. epididymis and seminal vesicles. and/or decrease in the number of testicular sperm heads were also found. Although histopathological changes such as atrophy of seminiferous tubules. loss or decrease of spermatogenic cells. exfoliation of spermatogenic cells. vacuolization of Sertoli cells. decrease of sperm. and/or increase of necrotic spermatogenic cells in epididymal ducts were observed. no adverse effects on the motility and morphology of epididymal sperm. copulation index. fertility index. and embryo-fetal development were detected in the 25 and 50 mg/kg groups. There were no evidences of male reproductive toxicity in the 12.5 mg/kg group. These results show that single intravenouse doses of DA-125 produce significant dose-related testicular atrophy. histopathological changes. and oligozoospermia in rats and $LD_{10}$ for DA-125 appears to be 50 mg/kg body weight.
Objectives : This research was executed to verify antitumor effect and protective effect on doxorubicin(Doxo)-induced toxicity of Cultivated Wild Ginseng(CWG) and synergic effect of CWG with Doxo in B16/F10 melanomas-bearing C57BL/6 mice. Methods : To evaluate protective effect on doxorubicin(Doxo)-induced toxicity and enhancing effect on the antitumor activity of Doxo, CWG water extract(0.5 ml) was intraperitoneally injected for 10 days, in combination with intraperitoneal injection of Doxo(4 mg/kg) on days 12, 16, 19, to mice subcutaneously inoculated with $2{\times}10^6/ml$ B16/F10 melanoma cells. In order to investigate antitumor effect of CWG, CWG water extract(0.5 ml) was intraperitoneally injected for 10 days to mice subcutaneously inoculated with $2{\times}10^6/ml$ B16/F10 melanoma cells. Results : The body weights of melanoma-bearing mice increased following B16/F10 cells inoculation. In contrast, such an increase in body weights was significantly attenuated by Doxo administration. Whereas CWG inhibits the decrease in body weights induced by Doxo. The tumor volume and tumor weights of melanomas-bearing mice dramatically increased following B16/F10 cells inoculation, In contrast, such an increase in tumor volume and tumor weights were significantly attenuated by Doxo or CWG administration. But the synergic effect of CWG with Doxo was not observed. The reduction of cellularity of seminiferous epithelia, level of spermatogonium and spermatid induced by Doxo was recovered by CWG administration. BrdU labeling index of spermatogonium was remarkably decreased in Doxo group but was no change in CWG group. Whereas the incidence and intensity of BrdU labelled spermatocytes and spermatids were increased by CWG administration than those of Doxo group. Conclusions : The obtained results suggest that CWG have antitumor effect and protective effect on doxo-induced testicular toxicity. This effect might be mediated through the supplementation of vital energy.
Oyeyipo, Ibukun P.;Skosana, Bongekile T.;Everson, Frans P.;Strijdom, Hans;du Plessis, Stefan S.
Toxicological Research
/
v.34
no.1
/
pp.41-48
/
2018
The efficacy of highly active antiretroviral therapy (HAART) has led to an increase demand for therapeutic use, thereby necessitating investigation into drug toxicity. This study was designed to investigate the in vivo effects of HAART on sperm parameters and testicular oxidative stress in lean and obese rats. Wistar rats (males, n = 40, weighing 180~200 g) were assigned randomly into 4 groups and treated accordingly for 16 weeks as follows: Control (C): lean group fed with standard rat chow; Diet induced obesity (DIO): obese animals fed a high caloric diet; C + ART: lean animals treated with HAART; DIO + ART: obese animals treated with HAART. An antiretroviral drug combination of Tenofovir, Emtricitabine and Efavirenz at a dose of 17, 26 and 50 mg/kg/day was administered for the latter 6 weeks via jelly cube feeding. At the end of the experimental period, sperm analysis was performed on sperm collected from the caudal epididymis, while the testis was homogenized for antioxidant enzyme and lipid peroxidation assays. Results showed that HAART significantly decreased sperm motility (p < 0.05) in both lean and obese animals, and viability (p < 0.05) in the DIO group. Testicular glutathione, catalase and superoxide dismutase were significantly decreased (p < 0.05), while Thiobarbituric acid reactive substances (TBARS) levels were significantly increased (p < 0.05) when the DIO+ART group was compared to Control group. Thus, the decreased sperm qualities associated with HAART might be as a result of increased testicular oxidative stress prominent in obese animals.
Kim, Jong-choon;Lee, Hyun-sook;Yun, Hyo-in;Chung, Moon-koo
Korean Journal of Veterinary Research
/
v.40
no.2
/
pp.361-371
/
2000
It has been recently reported that 2-bromopropane (2-BP) induces male reproductive toxicity in both human and experimental animals. However, delayed effects of 2-BP on male reproductive system have not been investigated in detail. The present study was conducted to investigate the testicular toxicity of 2-BP and to determine the recovery of normal spermatogenesis in Sprague-Dawley rats. Male rats aged 5 weeks were administered 1,000mg/kg 2-BP by gavage daily for 4 weeks and sacrificed sequentially at 1, 2, 3, 4 and 12 weeks after initiation of 2-BP treatment. Testicular toxicity was evaluated qualitatively by histopathological examinations and quantitatively by reproductive organ weights, spermatid head count, and repopulation index. In the 2-BP treated rats, the body weights was significantly suppressed and the weights of testes and epididymides were also decreased in a time-dependent manner. On histopathological examination, spermatogonia in stages I-VI and preleptotene and leptotene spermatocytes in stages VII-IX were strongly depleted at 1 week of dosing. Spermatogonia were depleted extensively in all spermatogenic stages at 2 weeks. Continuing with the evolution of spermatogenic cycle, zygotene spermatocytes, pachytene spermatocytes, and round spermatids were sequentially depleted at 2, 3, and 4 weeks of dosing due to the depletion of their precursor cells. Vacuolization of Sertoli cells and spermatid retention were also observed at all time points, suggesting that 2-BP induced Sertoli cell dysfunction. At 12 weeks, after 8 weeks recovery, most of the tubules appeared severely atrophic and were lined by Sertoli cells only. Leydig cell hyperplasia in the interstitial tissue was also found. In addition, dramatic reductions in the number of spermatid heads and repopulation index were observed, indicating that 2-BP-induced testicular injury is irreversible. These results indicate that 4 weeks repeated-dose of 1,000mg/kg 2-BP results in a progressive germ cell loss due to the depletion of spermatogonia followed by long-term testicular atrophy in SD rats.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.