In this study, the effect of brassinosteroid(BR) on the physiological and biochemical conditions of 2-year-old Panax notoginseng under the cadmium stress was investigated by the pot experiments. The results showed that cadmium treatment at 10 mg·kg~(-1) inhibited the root viability of P. notoginseng, significantly increased the content of H_2O_2 and MDA in the leaves and roots of P. noto-ginseng, caused oxidative damage of P. notoginseng, and reduced the activities of SOD and CAT. Cadmium stress reduced the chlorophyll content of P. notoginseng, increased leaf F_o, reduced F_m, F_v/F_m, and PIABS, and damaged the photosynthesis system of P. notoginseng. Cadmium treatment increased the soluble sugar content of P. notoginseng leaves and roots, inhibited the synthesis of soluble proteins, reduced the fresh weight and dry weight, and inhibited the growth of P. notoginseng. External spray application of 0.1 mg·L~(-1) BR reduced the H_2O_2 and MDA content in P. notoginseng leaves and roots under the cadmium stress, alleviated cadmium-induced oxidative damage to P. notoginseng, improved the antioxidant enzyme activity and root activity of P. notoginseng, increased the content of chlorophyll, reduced the F_o of P. notoginseng leaves, increased F_m, F_v/F_m, and PIABS, alleviated the cadmium-induced damage to the photosynthesis system, and improved the synthesis ability of soluble proteins. In summary, BR can enhance the anti-cadmium stress ability of P. notoginseng by regulating the antioxidant enzyme system and photosynthesis system of P. notoginseng under the cadmium stress. In the context of 0.1 mg·L~(-1) BR, P. notoginseng can better absorb and utilize light energy and synthesize more nutrients, which is more suitable for the growth and development of P. notoginseng.
Cadmium/metabolism* ; Antioxidants/pharmacology* ; Panax notoginseng ; Brassinosteroids/pharmacology* ; Chlorophyll/metabolism* ; Plant Roots/metabolism* ; Stress, Physiological

The well-known detrimental effects of cadmium (Cd) on plants are chloroplast destruction, photosynthetic pigment inhibition, imbalance of essential plant nutrients, and membrane damage. Jasmonic acid (JA) is an alleviator against different stresses such as salinity and drought. However, the functional attributes of JA in plants such as the interactive effects of JA application and Cd on rapeseed in response to heavy metal stress remain unclear. JA at 50 µmol/L was observed in literature to have senescence effects in plants. In the present study, 25 µmol/L JA is observed to be a "stress ameliorating molecule" by improving the tolerance of rapeseed plants to Cd toxicity. JA reduces the Cd uptake in the leaves, thereby reducing membrane damage and malondialdehyde content and increasing the essential nutrient uptake. Furthermore, JA shields the chloroplast against the damaging effects of Cd, thereby increasing gas exchange and photosynthetic pigments. Moreover, JA modulates the antioxidant enzyme activity to strengthen the internal defense system. Our results demonstrate the function of JA in alleviating Cd toxicity and its underlying mechanism. Moreover, JA attenuates the damage of Cd to plants. This study enriches our knowledge regarding the use of and protection provided by JA in Cd stress.
Brassica napus/metabolism* ; Cadmium/toxicity* ; Catalase/metabolism* ; Cyclopentanes/pharmacology* ; Oxylipins/pharmacology* ; Photosynthesis ; Plant Leaves/metabolism* ; Superoxide Dismutase/metabolism*

Effects of cadmium (Cd) on microbial biomass, activity and community diversity were assessed in a representative variable charge soil (Typic Aquult) using an incubation study. Cadmium was added as Cd(NO3)(2) to reach a concentration range of 0-16 mg Cd/kg soil. Soil extractable Cd generally increased with Cd loading rate, but decreased with incubation time. Soil microbial biomass was enhanced at low Cd levels (0.5-1 mg/kg), but was inhibited consistently with increasing Cd rate. The ratio of microbial biomass C/N varied with Cd treatment levels, decreasing at low Cd rate (<0.7 mg/kg available Cd), but increasing progressively with Cd loading. Soil respiration was restrained at low Cd loading (<1 mg/kg), and enhanced at higher Cd levels. Soil microbial metabolic quotient (MMQ) was generally greater at high Cd loading (1-16 mg/kg). However, the MMQ is also affected by other factors. Cd contamination reduces species diversity of soil microbial communities and their ability to metabolize different C substrates. Soils with higher levels of Cd contamination showed decreases in indicator phospholipids fatty acids (PLFAs) for Gram-negative bacteria and actinomycetes, while the indicator PLFAs for Gram-positive bacteria and fungi increased with increasing levels of Cd contamination.
Biomass ; Cadmium ; pharmacology ; Carbon ; metabolism ; Fatty Acids ; metabolism ; Microbial Viability ; drug effects ; Nitrogen ; metabolism ; Phospholipids ; metabolism ; Soil Microbiology ; Time Factors

OBJECTIVETo explore the effects of cadmium on zinc metabolism and its function and the protective effects of pre-supplement zinc to it.

METHODSNS or different doses of CdCl(2) were injected to pregnant dams intraperitoneally at the 7th, 10th and 13th day of gestation respectively. At the 21st pregnant day embryos were taken out from the pregnant rats. Another rats of pre-supplement zinc or no pre-supplement zinc group were injected different doses of CdCl(2) or NS intraperitoneally after 6 days. After 24 hours the rats were killed. The contents of Cd, Zn and relative biomarkers of effect of liver, brain or serum were detected in both embryos and adult rats.

RESULTSCompared with control group, the contents of T-AOC and Ach were significantly reduced in the Cd treatment group in the embryonic brains, the activity of AKP in the embryonic liver tissues was decreased, and The Cd content was increased significantly in embryonic liver and was negatively correlated with the Zinc content in the embryonic brain. There were no differences in the activities of SOD and AKP and the contents of Cd and MDA between pre-supplement Zn control group and no supplement Zn control group, but higher content of Zn in liver and serum in the former. Compared with no supplement Zn control group, there were higher contents of Cd in liver and serum, Zn and MDA in liver, lower activities of SOD in liver and AKP in liver and serum, and lower content of Zn in serum in the Cd treatment groups. Pre-supplement Zn significantly increase the content of Zn and the activities of SOD in liver and AKP in serum, decrease the content of MDA in liver and Cd in serum resulted by Cd treatment only. The content of Zn and the activity of AKP in serum and the activities of SOD and AKP in liver were negatively correlated with the content of Cd in corresponding tissue significantly.

CONCLUSIONCadmium can enter embryo and enter brain by permeating the brain-blood barrier during the embryonic period. The decrease of AKP activity, some neural transmitter and capacity of anti-lipid peroxidation that are related with Zn in embryos are caused when the pregnant rats are administered with cadmium. Cd can inhibits the activities of AKP and SOD in liver, and the activity of AKP in serum respectively, and increase the content of MDA in liver dose-dependently. The effects induced by cadmium are related with zinc abnormal distribution. Pre-supplement zinc to rats can antagonize these effects in different degree.

Animals ; Cadmium ; toxicity ; Female ; Liver ; metabolism ; Male ; Maternal Exposure ; Metallothionein ; metabolism ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Zinc ; metabolism ; pharmacology

Sedum alfredii Hance has been identified as zinc (Zn) and cadmium (Cd) co-hyperaccumulator. In this paper the relationships of Zn or Cd hyperaccumulation to the generation and the role of H2O2 in Sedum alfredii H. were examined. The results show that Zn and Cd contents in the shoots of Sedum alfredii H. treated with 1000 micromol/L Zn2+ and/or 200 micromol/L Cd2+ increased linearly within 15 d. Contents of total S, glutathione (GSH) and H2O2 in shoots also increased within 15 d, and then decreased. Total S and GSH contents in shoots were higher under Cd2+ treatment than under Zn2+ treatment. However, reverse trends of H2O2 content in shoots were obtained, in which much higher H2O2 content was observed in Zn2+-treated shoots than in Cd2+-treated shoots. Similarly, the microscopic imaging of H2O2 accumulation in leaves using H2O2 probe technique showed that much higher H2O2 accumulation was observed in the Zn2+-treated leaf than in the Cd2+-treated one. These results suggest that there are different responses in the generation of H2O2 upon exposure to Zn2+ and Cd2+ for the hyperaccumulator Sedum alfredii H. And this is the first report that the generation of H2O2 may play an important role in Zn hyperaccumulation in the leaves. Our results also imply that GSH may play an important role in the detoxification of dissociated Zn/Cd and the generation of H2O2.
Cadmium ; pharmacology ; Glutathione ; metabolism ; Hydrogen Peroxide ; metabolism ; Kinetics ; Plant Leaves ; metabolism ; Plant Shoots ; drug effects ; Sedum ; drug effects ; metabolism ; Sulfur ; metabolism ; Zinc ; pharmacology

OBJECTIVETo study the possible intervention of isoflavones in cytotoxicity induced by cadmium in vascular endothelial cells.

METHODSAn ECV 304 cell line derived from human umbilical vein endothelial cells was adopted. Genistein/daidzein was added prior to or simultaneously with CdCl2, cell viability was determined by MTT assay, and metallothionein mRNA expression was monitored by RT-PCR method.

RESULTSCell viability was higher in isoflavone and CdCl2 co-treated groups than that in CdCl2 treated group, with CdCl2 concentration at 10, 20, 40, and 80 micromol/L, respectively. However this increase was not observed in the group treated with CdCl2 at a concentration of 60 micromol/L. Isoflavones (10(-10) mol/L to 10(-5) mol/L) were added 24 h before cells were challenged with 80 micromol/L CdCl2 for 24 h or simultaneously with 80 micromol/L CdCl2. Genistein increased cell viability only at 10(-5) mol/L, while daidzein caused a dose-dependent increase from 10(-10) mol/L to 10(-5) mol/L in co-treatment with CdCl2. In pre-treatment, genistein (10(-7) to 10(-5) mol/L) increased cell viability whereas only 10(-5) mol/L of daidzein exerted protection. Apparent protection could be found when the cells were pre-treated with 10(-5) mol/L isoflavones for over 12 h, whereas 24 h incubation was required in such a co-treatment, with the exception of daidzein that had a significant protection in only 3 h. Isoflavones (10(-6) mol/L) incubated for 3 h to 24 h, increased MT IIA and MT IF mRNA expression, but the induction could not last for more than 24 h. Co-treatment with isoflavones could induce an additional induction of MT IIA mRNA expression in cells exposed to cadmium. However, the additional induction of MT IIA and MT IF mRNA was not seen when pre-treatment was carried out with isoflavones, with the exception of an increase in MT IIA mRNA expression in the daidzein pre-treated group.

CONCLUSIONGenistein/daidzein could reverse the cytotoxicity of cadmium either in pre-treatment or in co-treatment. The protection is the strongest in 10(-5) mol/L of isoflavones with a dose-dependent pattern. There are differences between genistein and daidzein in their protective effects. Whether the protection of isoflavones is related to their capacity of inducing MT mRNA expression remains to be elucidated.

Cadmium ; toxicity ; Cell Line ; Cell Survival ; drug effects ; Endothelial Cells ; drug effects ; metabolism ; Genistein ; pharmacology ; Humans ; Isoflavones ; pharmacology ; Metallothionein ; genetics ; metabolism ; Protective Agents ; pharmacology ; RNA, Messenger ; metabolism

Cadmium is known to exert toxic effects on multiple organs, including the testes. To determine if alpha-tocopherol, an antioxidant, could protect testicular tissues and spermatogenesis from the toxic effects of cadmium, six-week old male Sprague-Dawley rats were randomized to receive cadmium at doses of 0 (control), 1, 2, 4 or 8 mg/kg by the intraperitoneal route (Group A) or alpha-tocopherol for 5 days before being challenged with cadmium (Group B) in an identical dose-dependent manner. When both groups received cadmium at 1 mg/kg, there were no changes in testicular histology relative to controls. When Group A received cadmium at 2 mg/kg, undifferentiated spermatids and dead Sertoli cells increased in the seminiferous tubules while interstitial cells decreased and inflammatory cells increased in the interstitial tissues. On flow cytometric analysis, the numbers of elongated spermatids (M1) and round spermatids (M2) decreased while 2c stage cells (M3, diploid) increased. In contrast, when Group B received cadmium at 2 mg/kg, the histological insults were reduced and the distribution of the germ cell population remained comparable to controls. However, alpha-tocopherol had no protective effects with higher cadmium doses of 4 and 8 mg/kg. These findings indicate that alpha-tocopherol treatment can protect testicular tissue and preserve spermatogenesis from the detrimental effects of cadmium but its effectiveness is dependent on the dose of cadmium exposed.
alpha-Tocopherol/*pharmacology ; Testis/*drug effects/pathology ; Spermatogenesis/*drug effects ; Rats, Sprague-Dawley ; Rats ; Male ; Inflammation ; Flow Cytometry ; Dose-Response Relationship, Drug ; Cadmium Poisoning/*pathology ; Cadmium/metabolism/*pharmacology ; Antioxidants/pharmacology ; Animals

Animals ; Cadmium/toxicity* ; Dysbiosis/metabolism* ; Gastrointestinal Microbiome ; Glutamine/pharmacology* ; Methionine ; Mice ; Mice, Inbred C57BL ; Ostreidae ; Protein Hydrolysates ; Tyrosine

Cadmium (Cd) is a common heavy metal in the environment. Cd²⁺ may penetrate the blood-brain barrier and produce neurotoxicity, thus inducing various neurodegenerative diseases. Celastrol is an effective component of Tripterygium wilfordii Hook. F., which has many pharmacological effects such as anti-cancer and anti-inflammatory. Here we explored the effect of celastrol on the corresponding neurotoxicity induced by Cd²⁺. Cell proliferation test, cell membrane integrity test, and cell morphology were observed to analyze the effect of Cd²⁺ on the viability of HMC3. The neurotoxicity of Cd²⁺ and the effect of celastrol on the corresponding neurotoxicity induced by Cd²⁺ were analyzed by nitric oxide (NO) test, lipid peroxidation (MDA) test, and Western blotting. When the concentration of Cd²⁺ reached 40 μmol/L, the inhibition rate of HMC3 cell proliferation was (57.17±8.23)% (P < 0.01, n=5), compared with the control group. The cell activity continued to reduce when the Cd²⁺ concentration further increased. When the concentration of Cd²⁺ was higher than 40 μmol/L, the cell membrane of HMC3 was significantly damaged, and the damage was dose-dependent. Upon increasing the Cd²⁺ concentration, the cell morphology began to change and the adhesion also became worse. Cd²⁺ significantly increased the amount of NO released by HMC3 cells, while celastrol effectively inhibited the NO release of HMC3 cells induced by Cd²⁺. Cd²⁺ greatly increased the release of MDA in HMC3 cells, and the level of MDA decreased rapidly upon the addition of 10^-7 mol/L celastrol. Cd²⁺ increased the expression of p-PI3K protein, and the levels of p-PI3K protein and p-AKT protein were inhibited by the addition of celastrol (10^‒7 mol/L, 10^‒6 mol/L), thus preventing cell apoptosis. In conclusion, celastrol inhibits Cd²⁺ induced microglial cytotoxicity and plays a neuroprotective role.
Anti-Inflammatory Agents/pharmacology* ; Apoptosis ; Cadmium/toxicity* ; Nitric Oxide/pharmacology* ; Pentacyclic Triterpenes ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt/metabolism* ; Triterpenes/pharmacology*

OBJECTIVETo investigate the protective effect of sesamin against cadmium chloride (CdCl2)-induced cardiotoxicity in rats.

METHODSFifty male Wistar rats were randomly assigned to five groups: control group, CdCl2 group, and low-, middle-, and high-dose sesamin groups. The control group was given normal saline. The CdCl2 group and sesamin groups were intraperitoneally injected with CdCl2 (5 mg/kg×2 d), and the low-, middle-, and high-dose sesamin groups were given 20, 40, and 80 mg/kg sesamin, respectively. All treatments lasted for four weeks. ECG was measured by a physiological recorder, and serum myocardial enzyme levels were determined by biochemical assay. The heart was weighed, and heart tissues were used in histopathological examination and determination of malondialdehyde (MDA) level.

RESULTSCompared with the control group, the CdCl2 group showed significantly higher levels of serum CK and CK-MB, an increased heart coefficient, significant ST-segment elevation, and higher level of MDA in myocardial tissue (P < 0.05). Histopathological analysis showed edema of myocardial tissues and cells, myocardial fibers disorder, karyopyknosis, and uneven or deep staining of nuclear chromatin. Different doses of sesamin relieved the myocardial pathological changes induced by CdCl2, and high-dose sesamin was the most effective. The middle- and high-dose sesamin groups showed significantly reduced serum CK and CK-MB levels compared with the CdCl2 group (P < 0.05). The heart coefficient of the high-dose sesamin group (0.19±0.01%) was significantly lower than that of the CdCl2 group (0.21±0.01%) (P < 0.05). Myocardial MDA levels of the three sesamin groups (42.32±4.65, 36.71±5.34, and 33.12±4.62 nmol/mg pro, respectively) were all significantly lower than that of the CdCl2 group (55.87±3.65 nmol/mg pro) (P < 0.05).

CONCLUSIONSesamin can relieve myocardial injury induced by CdCl2, and one possible mechanism is the enhancement of antioxidant capacity of myocardial tissue.

Animals ; Cadmium Chloride ; toxicity ; Creatine Kinase, MB Form ; blood ; Dioxoles ; pharmacology ; Heart ; drug effects ; Lignans ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Wistar