AIM: To better clarify the main target organs of dimethylarsinic acid toxicity and the role of metallothionein (MTs) in modifying dimethylarsinic acid (DMAA) toxicity. METHODS: MT-Ⅰ/Ⅱ null (MT^-/-) mice and the corr...AIM: To better clarify the main target organs of dimethylarsinic acid toxicity and the role of metallothionein (MTs) in modifying dimethylarsinic acid (DMAA) toxicity. METHODS: MT-Ⅰ/Ⅱ null (MT^-/-) mice and the corresponding wild-type mice (MT^+/+), six in each group, were exposed to DMAA (0-750 mg/kg body weight) by a single oral injection.Twenty four hours later, the lungs, livers and kidneys were collected and undergone pathological analysis, induction of apoptolic cells as determined by TUNEL and Mr concentration was detected by radio-immunoassay. RESULTS: Remarkable pathological lesions were observed at the doses ranging from 350 to 750 mg/kg body weight in the lungs, livers and kidneys and MT^+/+ mice exhibited a relatively slight destruction when compared with that in dose matched MT/ mice. The number of apoptotic cells was increased in a dose dependent manner in the lungs and livers in both types of mice. DMAA produced more necrotic cells rather than apoptotic cells at the highest dose of 750 mg/kg,however, no significant increase was observed in the kidney.Hepatic Mr level in Mr^+/+ mice was significantly increased by DMAA in a dose-dependent manner and there was no detectable amount of hepatic MT in untreated MT^-/- mice. CONCLUSION: DMAA treatment can lead to the induction of apoptosis and pathological damage in both types of mice.MT exhibits a protective effect against DMAA toxicity.展开更多
Aim: To clarify the immuno-active LH (i-LH) and bioactive LH (b-LH) responses and qualitative changes in the cir-culating LH to testosterone undecanoate (TU) injection. Methods: Eight men with Klinefelter's syndro...Aim: To clarify the immuno-active LH (i-LH) and bioactive LH (b-LH) responses and qualitative changes in the cir-culating LH to testosterone undecanoate (TU) injection. Methods: Eight men with Klinefelter's syndrome were re-cruited for the study. They received crossover injections of TU at doses of 500 and 1000 mg. Serum i-LH and b-LHlevels before and at various time intervals after TU injection were measured and the serum i-LH, b-LH, b-LH/i-LH(B/I) and testosterone/sex hormone-binding globulin (T/SHBG) ratio in LH-responders and LH non-responders werecompared. Results: A parallel suppression of serum i-LH and b-LH was consistent with their overall high correlationbetween each other ( r = 0.84, P < 0. 001). Mean serum i-FSH levels were decreased by TU injection at both doseswithout dose-response effects. LH-responders had lower baseline serum i-LH and b-LH, and higher E_2 levels and T/SHBG ratio. There was a quantitative change in serum LH as induced by TU without qualitative change within LH-re-sponders os LH-non-responders. Conclusion: A high loading dose (1000 mg) of TU is important for the initial sup-pression of LH. With the lower dose (500 mg), repeated injections will be required to attain such LH suppression forthe purpose of fertility regulation. The lower baseline serum i-LH level may be an intrinsic characteristic of LH-respon-ders.展开更多
文摘AIM: To better clarify the main target organs of dimethylarsinic acid toxicity and the role of metallothionein (MTs) in modifying dimethylarsinic acid (DMAA) toxicity. METHODS: MT-Ⅰ/Ⅱ null (MT^-/-) mice and the corresponding wild-type mice (MT^+/+), six in each group, were exposed to DMAA (0-750 mg/kg body weight) by a single oral injection.Twenty four hours later, the lungs, livers and kidneys were collected and undergone pathological analysis, induction of apoptolic cells as determined by TUNEL and Mr concentration was detected by radio-immunoassay. RESULTS: Remarkable pathological lesions were observed at the doses ranging from 350 to 750 mg/kg body weight in the lungs, livers and kidneys and MT^+/+ mice exhibited a relatively slight destruction when compared with that in dose matched MT/ mice. The number of apoptotic cells was increased in a dose dependent manner in the lungs and livers in both types of mice. DMAA produced more necrotic cells rather than apoptotic cells at the highest dose of 750 mg/kg,however, no significant increase was observed in the kidney.Hepatic Mr level in Mr^+/+ mice was significantly increased by DMAA in a dose-dependent manner and there was no detectable amount of hepatic MT in untreated MT^-/- mice. CONCLUSION: DMAA treatment can lead to the induction of apoptosis and pathological damage in both types of mice.MT exhibits a protective effect against DMAA toxicity.
文摘Aim: To clarify the immuno-active LH (i-LH) and bioactive LH (b-LH) responses and qualitative changes in the cir-culating LH to testosterone undecanoate (TU) injection. Methods: Eight men with Klinefelter's syndrome were re-cruited for the study. They received crossover injections of TU at doses of 500 and 1000 mg. Serum i-LH and b-LHlevels before and at various time intervals after TU injection were measured and the serum i-LH, b-LH, b-LH/i-LH(B/I) and testosterone/sex hormone-binding globulin (T/SHBG) ratio in LH-responders and LH non-responders werecompared. Results: A parallel suppression of serum i-LH and b-LH was consistent with their overall high correlationbetween each other ( r = 0.84, P < 0. 001). Mean serum i-FSH levels were decreased by TU injection at both doseswithout dose-response effects. LH-responders had lower baseline serum i-LH and b-LH, and higher E_2 levels and T/SHBG ratio. There was a quantitative change in serum LH as induced by TU without qualitative change within LH-re-sponders os LH-non-responders. Conclusion: A high loading dose (1000 mg) of TU is important for the initial sup-pression of LH. With the lower dose (500 mg), repeated injections will be required to attain such LH suppression forthe purpose of fertility regulation. The lower baseline serum i-LH level may be an intrinsic characteristic of LH-respon-ders.
