• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.4
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• pp.782-787
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• 2002

This study was carried out to investigate the protective effect of chitosan on lipid peroxidation and key lipid parameters in Sprague-Dawley rat (SO rat) accutely exposured to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Male SO rats received single intraperitoneal (ip) injection of TCDD (40 j.lg/kg), and were given diet containing 3 or 5% chitosan for 4 weeks from 1 week before TCDD treatment. The gain in body weight was less in group treated with TCDD than in CON group, while that of Ch/H+ TCDD group (5% chitosan diet) increased. The decrease in liver and testis weight caused by TCDD was prevented by high dietary intake of chitosan (5% chitosan). Serum (total cholesterol, triglyceride, HDL-C, and LDL-C) and liver lipid parameters (total lipid, total cholesterol, and triglyceride) were significantly elevated in TCDD-induced rats, but these parameters excluding HDL-C were significantly reduced in high dietary intake of chitosan (5% chitosan). These findings suggest that chitosan is believed to be a possible protective effect against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rat.

• Environmental Analysis Health and Toxicology
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• v.24 no.1
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• pp.1-8
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• 2009

In this study, we obtained the fertilized eggs from goldfish(Carassius auratus) and observed normal developmental stage(from fertilized eggs to larvae) in non-exposed groups. Goldfish embryos at 3 h postfertilization(hpf) were statically exposed for 1 h to either dimethylsufoxide(DMSO, 0.1%, v/v) or TCDD($0.5{\mu}g/L$). Toxicity and morphological changes were characterized from 3 to 120 h postfertilization(hpf). Egg mortality($0{\sim}48$ hpf) and hatching ratio($72{\sim}83$ hpf) in TCDD-exposed group were significantly different from control groups. However, pericardial edema was first observed at 72 hpf, followed by the onset of yolk sac edema and mortality. In addition, goldfish embryos-larvae exposed to TCDD significantly increased TCDD-related gene such as CYP1A($24{\sim}72$ hpf) and AhR2(72 hpf). This is the first study about in-depth characterization of TCDD-induced developmental toxicity in goldfish(Carassius auratus).

• Journal of Environmental Health Sciences
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• v.28 no.2
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• pp.131-139
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• 2002

초기생애단계의 일본송사리를 실험어류로 사용하여 TCDD와 PCB 126의 생물농축정도를 비교 측정하였고, TCDD와 PCB 126의 체외 배설에 대한 동태학적 특성을 비교 분석하였다. 생물농축실험은 초기생애단계의 새끼치어 및 어린 물고기에 TCDD와 PCB 126을 여러 농도로 물에 용해시켜 96시간 동안 정체된 상태로 폭로시킨 후 생물농축계수(BCF)와 지방-표준화한 생물농축계수(BCF$_{L}$)를 측정하였다. TCDD와 PCB 126의 일본송사리 초기생애단계의 새끼치어 및 어린 물고기에서 측정된 96-h BCF값 및 96-h BCF$_{L}$값은 폭로된 농도와 상관없이 비슷하게 나타나 반면, 생체크기가 클수록 그 값은 작게 나타났다. 일본송사리 새끼치어, 어린 물고기, 성어의 생체 내 총 지방함량은 각각 5.7, 4.2, 4.6%로 측정되었다. 체외배설 동태실험은 어린 물고기에 TCDD와 PCB 126을 3가지 농도롤 물에 용해시켜 96시간 동안 정체된 상태로 폭로시킨 후, flow-through장치로 공급되는 맑은 물로 옮겨 42일간 사양하면서 0, 7, 14, 21, 28, 42일에 생체 내 TCDD와 PCB 126 잔류량을 측정하여 분석하였다. 배설은 1차 반응속도론적으로 이루어졌으며 한 구획모형보다 두 구획모형이 더 적합한 것으로 분석되었다. 두 구획모형을 사용한 분석에서 TCDD와 PCB 126의 체외배설 반감기(t$\frac{1}{2}$) 및 배설속도상수($\beta$)는 각각 27.2일과 32.3일 및 0.025/d와 0.021/d로 측정되었다.

• Environmental Mutagens and Carcinogens
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• v.24 no.2
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• pp.91-98
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• 2004

Although 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) is a powerful carcinogen in several species, limited model system exist to study carcinogenicity of this compound at cellular level. To enhance our under-standing of carcinogenicity of TCDD at cellular level, we investigated micronucleus (MN) frequency as a index of genetic toxicity and whether TCDD can transform the human cells in culture. Normal human cell lines, skin keratinocyte HaCaT, Chang liver and breast MCF10A cells were used. TCDD did not affect the cell viability of the Chang liver, HaCaT and MCF10A cells. The frequency of micronucleus was increased after treatment of TCDD for 24hr in Chang liver and HaCaT cells, but not changed in MCF10A cells. And we observed putative transformed cells in Chang liver cells exposed to 1 $\mu$M TCDD for 2 weeks. The putative transformed cells were also observed in HaCaT cells with subsequent exposure to TCDD (0.1, 1, 10, 100 nM) for 2 weeks after initial exposure to MNNG, but not observed in MCF10A cells. Collectively, these results indicate that the ability of TCDD to induce micronuclei may be involved in cellular transformation of Chang liver and HaCaT cells. Our putative TCDD-transformed cells of Chang liver and HaCaT are expected to provide a clue to the elucidation of TCDD-induced transformation pathway.

• Korean Journal of Clinical Laboratory Science
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• v.36 no.2
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• pp.258-268
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• 2004

This study was carried out to investigate preventive effects of extracts of cricket, Gryllus bimaculatus, against the 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD)-induced toxicity in 7-week-old Sprague-Dawley male rats. Thirty five male rats were divided into 5 groups: one normal control group treated with vehicle and saline (G1); one TCDD-treated group by single intraperitoneal injection (G2); three preventive groups (G3, G4, and G5). The last three groups, G3, G4, and G5, were fed on cricket extracts (50, 100, and 200 mg/kg, respectively) for 2 weeks before TCDD treatment. Various harmful effects were shown by TCDD treatment. The body weights of rats were lost by TCDD. In addition, severe hypertrophy and color change, and the weights gaining were found in the livers of TCDD-treated rats. It was observed that the cytoplasmic vacuolizations and inflammatory cell infiltration around portal triad in the liver. TCDD also elevated the serum activity levels of alanine transaminase(ALT) and aspartate transaminase(AST). However, those losses were compensated by cricket extracts treatment at the level of 200 mg/kg. These findings indicate that cricket extracts may have protective effects against TCDD-induced toxicities in rats.

• Environmental Analysis Health and Toxicology
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• v.25 no.3
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• pp.241-251
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• 2010

Crucian carp (Carassius auratus) has been used as the sentinel species for POPs (Persistent Organic Pollutants) monitoring in aquatic environment. However, there is little information for dioxin toxicity and especially, early life stage toxicity in crucian carp have been never carried out. In this study, we investigated several toxic effects for 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in fertilized egg obtained by natural fertilization from crucian carp. The embryos at 3 h post-fertilization (hpf) were treated with 0.039, 0.156, 0.625, and 2.5 (${\mu}g/L$) TCDD by waterborne exposure for 60 minutes and changed with fresh water 2 times per day. Fertilized eggs started hatching at 51 hpf and TCDD exposed embryo showed decrease of hatching rate in a dose-dependent manner at 75 hpf. Pericardial edema was continuously observed in larvae exposed to TCDD from hatching start time (51 hpf), followed by the onset of mortality. In addition, AhR-related gene, CYP1A was clearly increased by TCDD in a dose dependent manner. These results indicated that fertilized eggs obtained from crucian carp have the TCDD related gene regulation and a distinct TCDD developmental toxicity syndrome by TCDD exposure. Therefore, we suggested that early life stage test in crucian carp could be used as test methods on dioxins toxicity.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.211.2-211.2
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• 2003

Saururus Chinensis Baill (Saururaceae) has been used as folk medicine for analgesics, beriberi, edema, hepatitis, and icterus, etc. Hepatoprotective effects of Saururus chinensis Baill (SCB) administration on function of the biochemical parameters in liver of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treated rats were investigated. After 7 days from TCDD(1$\mu\textrm{g}$/kg) injection, SCB(200mg/kg) was administered into rats intraperitoneally for 4 week.s We examined the antioxidative enzymatic activity by measuring the level of AST and ALT in serum and SOD, Catalase, GPx, GSH and GSSG in liver tissue of rats. (omitted)

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.94-94
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• 2003

Endocrine disrupters (EDs) are exogenous chemicals that interfere with the production, releasing, metabolism, excretion, binding of natural hormones, and whole endocrine systems. EDs are very dangerous since they are extremely stable, not easily degraded, and accumulated in fat and tissue. 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) is known as the most toxic EDs. Therefore, this study was conducted to investigate the effects of TCDD on proliferation of human breast cancer (MCF-7) and endometrial adenocarcinoma (Hec-1B) cells. 10, 100, and 1000 nM of TCDD were treated with steroid free condition. Viable cell counting, MTT, and BrdU assay was performed to investigate cell proliferation. Apoptosis was investigated using DNA laddering. Although, DNA fragmentation as the evidence of apoptosis was not detected, all of these cell lines showed restricted proliferation at 48 hrs after 100 and 1000 nM TCDD treatments. Recently, it has been reported that the expression of transforming growth factor $\beta$s (TGF-$\beta$s) are increased in TCDD treatment and also involved in regulation of cell cycle. Therefore, these results were considered that the decreased cell prolifcration by TCDD is related to the expression of TGF-$\beta$s.

• Journal of Nutrition and Health
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• v.38 no.9
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• pp.689-697
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• 2005

This study was conducted to fine out the preventive effects of chitosan and chitosan oligomer on the disorders of hepatic functions and lipid metabolism induced by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) using adult male rats (SD) for four weeks. Rats were fed chitosan ($4\%$) or chitosan oligomer ($4\%$) diets respectively before 3weeks of TCDD treatment (50 ug/kg BW) by intraperitoneal injection and then continually supplied these diets for one week until being sacrificed. The elevation of serum total and LDL cholesterol levels induced by TCDD treatment was significantly reduced in the rats fed chitosan diets. The increment of liver triglyceride levels caused by TCDD treatment was tended to suppress in all rats fed chitosan and chitosan oligomer diets. Fecal total lipid and cholesterol excretion were high levels in the rats fed chitosan diets. The hepatic cytosolic catalase activities significantly decreased by TCDD treatment appeared recovering trend by chitosan diets. In hepatic microsomal cytochrome p-450, NADPH cytochrome p-450 reductase, ethoxycoumarin-o-deethylase (ECOD) and benzphetamin N-demethylase (BPND) chitosan than chitosan oligomer diets apparently decreased the increasing levels by TCDD treatment. In histochemical observation the fat droplets and apoptosis of hepatocytes by TCDD treatment were markedly alleviated by chitosan and chitosan oligomer diets. These results indicate that chitosan, more than chitosan oligomer can exert preventive effects on some disorders of hepatic functions and lipids accumulation by TCDD.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.8
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• pp.1169-1174
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• 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.