Mercuric chloride effects on adult rat oval cells-induced apoptosis

In the present investigation, the toxicity of mercuric chloride (HgCl₂) was evaluated in adult oval cells isolated from rat utilizing the 2-acetylaminofluorene/partial hepatectomy technique. Isolated oval cells were incubated with 5 μM of HgCl₂ for 8 hr to elucidate in vitro cytotoxic responses. Recently, autophagic cell death was found in rat hepatocytes in vitro within 30 min of incubation with 5 μM of mercury (Hg) which triggered apoptosis and necroptosis in a time-dependent manner. Nuclear degradation occurred within 30 min of incubation and progressed with time until 8 hr. Apoptosis evidenced by activation of caspase-dependent pathway between 30 min to 8 hr of incubation was mediated via interchange of death domain signaling pathways. Receptor-interacting protein played a positive role to modulate the death domain receptors in the scenario of apoptotic death of oval cells until 6 hr. Autophagic marker proteins ATG12 and LC3B exerted a significant role in triggering apoptosis in 5 μM Hg-treated oval cells. No apparent expression of apoptosis-inducing-factor (AIF) and HMGB1 indicated absence of caspase-independent apoptosis and necrosis in the rat oval cells between 30 min and 8 hr. Thus a low concentration of Hg modulates programmed cell death in adult rat oval cells by altering expression of proteins involved in the molecular mechanisms of cellular functions.     

Protective role of Curcuma longa extract and curcumin on mercuric chloride-induced nephrotoxicity in rats: evidence by histological architecture

Mercury (Hg) is a potent nephrotoxin. The aim of this study was to investigate the protective role of Curcuma longa extract and curcumin against HgCl₂-induced nephrotoxicity. Male Sprague Dawley rats were administered HgCl₂ (12 μmol kg^?1, ip; once only) followed by treatment of Curcuma longa extract (200 mg kg^?1, po) and curcumin (80 mg kg^?1, po) for three days after 24 h of HgCl₂ administration. The present results showed that mercuric chloride administration caused an impairment of renal function system which was evident from significant increase in urea, creatinine, uric acid, and blood urea nitrogen concentration in serum. In addition, the swelling in glomerulus and degenerated renal tubules with obstructed lumen was also observed by acute mercuric chloride administration. Treatment with Curcuma longa extract and curcumin was effective in restoring all variables of kidney functions near to control group, which was consistent with kidney histoarchitecture. In conclusion, these results suggest that Curcuma longa extract and curcumin protect against HgCl₂-induced nephrotoxicity. This study could be important for the further understanding of mercury toxicity in renal tissues and in the development of better treatments for people and/or animals exposed to the metal.     

Protective role of epigallocatechin 3-gallate against lead-induced toxicity in human neuroblastoma cells

Lead (Pb) is a heavy metal, known to induce oxidative stress and produce damage to the antioxidant defence system ultimately leading to cell death. Antioxidants such as epigallocatechin 3-gallate (EGCG), a green tea polyphenol, was shown to play a protective role during Pb-exposure. In this study, human SH-SY5Y neuroblastoma cells were exposed to different concentrations (0.01–10?µM) of Pb for 48?h to determine effects on the viability of cells. It was observed that IC₅₀ was at 5?µM and at this concentration the cells exhibited a significant increase in caspase-3 activity, an indicator of apoptosis at least by 10-fold and the decrease of 59.4% in glutathione (GSH) content. The total cellular prostaglandin-E₂ (PGE₂) level was found to be elevated at least 10-fold upon Pb exposure. However, the effects of Pb on cells pre-incubated with 50?µM EGCG followed by 5?µM Pb showed 40% inhibition in cell viability, 17.3% decrease in caspase-3 activity, 23% increase in GSH content, and 11.4% fall in PGE₂ levels when compared with cells exposed to Pb only. Data suggest that EGCG exerted a significant protection to cell viability in preventing cell death and elevation in levels of GSH in cells exposed to Pb. However, EGCG did not elicit any significant effect on release of PGE₂ indicating the nature of EGCG as an effective anti-apoptotic, antioxidant, and anti-inflammatory agent.     

Regulation of autophagy in rat hepatocytes treated in vitro with low concentration of mercury

Several proteins are implicated in the regulation of autophagy in cells under various physiological and pathological conditions. Recently it was found that in vitro initiation of autophagy in 5 μM mercuric chloride (HgCl₂) treated rat hepatocytes occurred within 30 min of incubation. The aim of this study was to monitor the autophagy–ubiquitination link to determine the regulatory mechanisms underlying autophagy at a concentration of 5 μM HgCl₂. Autophagic cell death was evidenced by the presence of LC3B positive hepatocytes throughout the incubation period of 4 hr. Autophagosome maturation occurred following 1 hr of metal treatment accompanied by an enhanced expression of several regulatory proteins such as p62, Keap1, and caspase-8, which drive the hepatocytes toward autophagy. In addition, the rate of increase in down-regulation in a p38 expression was significantly higher than that of extracellular signal-regulated kinase (ERK) at 1 hr incubation, followed by a significant decline in the p38 level at 2 and 4 hr following metal treatment. In contrast, the expression of ERK remained higher than that of p38 at 2 and 4 hr. Data indicate that intracellular activation of the major regulatory proteins such as LC3B, caspase-8, Keap1, p62, ERK, and p38 modulates autophagy through ubiquitination in rat hepatocytes exposed to low concentrations of Hg.     

Mercuric chloride induced proteotoxicity and structural destabilization in marine fish (Therapon jarbua)

The reaction byproducts derived from lipid peroxidation (LPO), as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) enzyme activities were measured in tissues of marine fish (Therapon jarbua) exposed to mercuric chloride (HgCl) in water dispersions of 0.125 or 0.25 ppm. LPO was significantly increased in various tissues relative to control values after 96-h exposure. SOD and GPx activities significantly decreased after exposure to first two doses but significantly elevated CAT in Dose II kidney and liver tissues. The elevated levels of LPO, decreased activities of SOD and GPx, and increased CAT activities in all tissues examined in T. jarbua are an index of oxidative stress in fish. Structural analysis by scanning electron microscopy studies revealed the structural deformation in HgCl₂-exposed animals. These observations suggest that HgCl acts as a mediator in free radical generation. The increase in CAT and decrease in SOD and GPx activities in these tissues may be an adaptive response.     

Determination of cytotoxic,genotoxic, and oxidative damage from deltamethrin on primary hepatocyte culture of Lake Van fish,Alburnus tarichi

ABSTRACT

Deltamethrin is a widely used pyrethroits worldwide. Although the chemical is used to combat insects, it has effects on other non-target organisms. Deltamethrin is extensively used in agriculture, animal husbandry, and domestic areas in the Lake Van basin. The aim of this study was to determine the cytotoxic, genotoxic, and oxidative damage from deltamethrin on the primary hepatocyte culture of Lake Van fish (Alburnus tarichi). In this study, the toxic effects of different concentrations (0.01, 0.1, 1, and 10?µM) of deltamethrin in the primary hepatocyte culture of Lake Van fish were investigated via liver enzymes aspartase aminotransferase (AST) and alanine aminotransferase (ALT), and the total antioxidant status (TAS), total oxidant status (TOS), lipid peroxidation (MDA), and DNA damage (8-OHdG).

Deltamethrin caused an increase in the AST and ALT levels dependent on the dosage and time. The TAS and TOS levels increased at the end of 24?h and there was no difference at the end of 48?h. Deltamethrin did not affect the MDA level, but increased the 8-OHdG (P?<?0.05). In conclusion, it can be said that high doses of deltamethrin (1 and 10?µM) have a toxic effect on the primary hepatocyte culture of Lake Van fish.     

Accumulation,tissue distribution and elimination of 203HgCl2 and CH3 203HgCl in the tissues of the American oyster Crassostrea virginica

Oysters (Crassostrea virginica) were exposed for 3 days to mercury-203 labeled HgCl₂ or CH₃HgCl added directly to artificial seawater or added preconcentrated on the marine diatom Phaeodactylum tricornutum. The concentration of mercury in 5 tissues was measured for 45 days after mercury was removed from the ambient water. At the beginning of the depuration period, the highest concentrations of mercury in tissues were attained in: gill>digestive system>mantle>gonad>muscle in oysters exposed to water containing mercury; and in digestive system>gill>mantle> gonad>muscle in oysters fed labeled algae. This same distribution pattern is seen for both chemical forms of mercury. Although the initial pattern of accumulation was identical for both mercury compounds within each exposure group, the fate of the accumulated mercury was very different after 45-days depuration. In oysters accumulating mercury directly from seawater, inorganic mercury residues rapidly declined in gill and digestive tissue, but were slowly reduced in mantle, gonadal, and muscle tissue. This pattern was duplicated by oysters exposed to methyl mercuric chloride in seawater except that gonadal and muscle residues greatly increased during depuration. In oysters ingesting labeled P. tricornutum cells, mercuric chloride and methyl mercuric chloride residues rapidly declined in gill and digestive tissue, remained constant in the mantle, but sharply increased in gonadal and muscle tissue during depuration.     

Effects of sublethal concentrations of mercuric chloride on ammonium-limitedSkeletonema costatum

The effect of sublethal additions of mercuric chloride on the marine diatomSkeletonema costatum (Grev.) Cleve grown in NH₄-limited chemostats and batch cultures was assessed. In short-term Hg exposure experiments (up to 5 h), the effect of Hg on ammonium uptake rates was studied by simulatneously perturbing the culture with 5 M NH₄ Cl and Hg concentrations ranging from 0.04 to 5.52 nM HgCl₂. The threshold of Hg toxicity occurred between 1.8 and 3.7 nM, based on a decrease in ammonium uptake rates. When the NH₄-limited culture was starved of ammonium for 30 h, the threshold of Hg toxicity decreased about an order of magnitude to 0.2 nM. In long-term Hg exposure experiments (679.5 h), NH₄-limited continuous cultures were semi-continuously exposed to 0.37 and 3.68 nM HgCl₂. After 4 days, the cell density in the Hg-treated chemostats began to drastically decline. After about 16 days these populations recovered, even though Hg additions continued. At the end of the experiment (26 days), cell densities had reached the levels observed at the beginning of the experiment. The reason for the recovery is unknown, but several possibilities are discussed. Ammonium uptake rates determined during the time-course of this long-term Hg exposure, indicated that these NH₄-limited cultures exhibited a significant loss in their ability to take up ammonium at low concentrations (e.g. 1 M). Thus, mercury pollution may seriously decrease the ability of a species to utilize the limiting nutrient during periods of seasonal nutrient limitation.     

Cytotoxicity of benalaxyl,metalaxyl, and triadimefon on Chinese hamster ovary cells

The cytotoxicity of the fungicides benalaxyl, metalaxyl, and triadimefon was evaluated in vitro using the Chinese hamster ovary (CHO-K1) cell line. The midpoint cytotoxicity values of neutral red (NR) incorporation (NRI₅₀), total cellular protein content (TCP₅₀), and the methyl tetrazolium assay (MTT₅₀) were estimated. Benalaxyl was the most cytotoxic fungicide, followed by metalaxyl and triadimefon. Fetal calf serum (10%) caused a reduction in benalaxyl, metalaxyl, and triadimefon cytotoxicity by factors of 1.8, 1.3, and 1.3. The effects of sublethal concentrations (NRI₂₅) of the three fungicides on the glutathione redox cycle components glutathione S-transferase, glutathione reductase, glutathione peroxidase, and total glutathione content were studied. The ameliorative effects of extracellular glutathione (1 mmol L^?1), vitamin C (70 µmol L^?1), and vitamin E (30 µmol L^?1) were also investigated. The three antioxidants led to significant effects on the glutathione redox cycle components.     

In vitro assessment of natural plant extracts Withania somnifera,Cassia fistula,Saraca asoca,and Eucalyptus tereticornis using primary chicken embryo fibroblast cell culture treated with urea or mercuric chloride (II)

The present investigation examined the detoxifying potential of methanolic herbal extracts, namely the leaf and bark extract of Eucalyptus tereticornis, bark extract of Saraca asoca, Cassia fistula and Withania somnifera in vitro using primary chicken embryo fibroblast (CEF) cells against damaging effects of urea and mercuric chloride (HgCl) (II). The influence of 20?mM urea and 10?µM?HgCl (II) was determined on cell viability or proliferation of cells after treatment with plant extracts. Higher survival rate of primary CEF cells treated with higher concentrations of plant extracts was observed due to their protective ability against urea and HgCl (II). Cassia fistula bark extract (10?mg?mL^?1) was found to be most effective against 20?mM urea as it protects 90% of CEF cells whereas W. somnifera protects 86% of the cells within 24?h. After treating cells with10?µM HgCl, W. somnifera and E. tereticornis leaf extracts were found to be more effective among all other extracts as they protect approximately 86% and 70% of CEF cells, respectively, within 24?h. These results indicate that C. fistula and W. somnifera has the highest potential amongst all the five plant extracts for protecting CEF cells against damaging effects of urea and HgCl (II), respectively.     

Differential effects of UV-B radiation fluence rates on growth,photosynthesis, and phosphate metabolism in two cyanobacteria under copper toxicity

This work was undertaken to ascertain the impact of different fluence rates of ultraviolet-B (UV-B) radiation on two cyanobacterial biofertilizers, Phormidium foveolarum and Nostoc muscorum, growing under copper toxicity. Copper (2 and 5?µmol?L^?1) and high UV-B fluence rate (UV-B_H; 1.0?µmol?m^?2?s^?1) decreased the growth, pigment content, photosynthetic oxygen yield, phosphate uptake, and acid phosphatase activity in both the strains analyzed after 24 and 72?h of experiments, and combined exposure further enhanced the toxic effects. Respiration and alkaline phosphatase activities were stimulated appreciably. The damaging effect was shown on the order on pigments: phycocyanin?>?chlorophyll a?>?carotenoids, and on photosystems: whole chain photosynthetic reaction?>?photosystem II?>?photosystem I. Partial recovery in the photosystem II activity in the presence of artificial electron donors; diphenyl carbazide (DPC), hydroxylamine (NH₂OH), and manganese chloride (MnCl₂) pointed out the interruption of electron flow on the oxidation side of photosystem II. Unlike UV-B_H, low UV-B fluence rate (UV-B_L; 0.1?µmol?m^?2?s^?1), rather than causing damaging effect partially, alleviated the toxic effects of Cu. This study suggests that the cyanobacterium P. foveolarum is less sensitive against UV-B_H and excess Cu (2 and 5?µmol?L^?1), thus P. foveolarum may be used as a biofertilizer for sustainable agriculture.     

Effects of vanadate supply on plant growth, Cu accumulation, and antioxidant capacities in Triticum aestivum L.

The effects of normal vanadate (V) supply (40 μM) on copper (Cu) accumulation, plant growth and reduction in Cu toxicity in wheat seedlings (Triticum aestivum L.) were investigated. The results showed Cu accumulation (mg g^?1 dw) in the applied V treatment was about 10.2 % in shoots and 16.7 % in roots higher up on exposure to excess Cu (300 μM) than that observed only in excess Cu plants. Compared with the treatment of the normal concentration used in Hoagland’s culture solution Cu (0.6 μM), excess Cu significantly induced lipid peroxidation indicated by accumulation of thiobarbituric acid reactive substances (MDA). The seedlings showed apparent symptoms of Cu toxicity and plant growth were significantly inhibited by excess Cu. The applied V significantly decreased lipid peroxidation in roots caused by excess Cu and inhibited the appearance of Cu toxicity symptoms. Moreover, the applied V effectively improved the antioxidant defense system to alleviate the oxidative damage induced by Cu. Although the addition of V could promote superoxide dismutase in both shoots and roots to reduce superoxide radicals, peroxidase and catalase in shoots and ascorbate peroxidase and dehydroascorbate reductase in roots were major enzymes to eliminate H₂O₂ in wheat seedlings.     

Ameliorating effects of hormone and Cu on salt stressed Brassica nigra (L.) Koch with reference to growth and biochemical characteristics

The ameliorating effects of exogenous hormone and calcium were investigated in salt-stressed black mustard seedlings (Brassica nigra L.). The seedlings were subjected to various treatments: control (nutrient solution), salt stress, kinetin/abscisic acid (ABA)/calcium chloride (CaCl₂). Sodium chloride (NaCl) inhibited shoot length (45–55%) and root (<75%). Further, alterations in superoxide dismutase and catalase activities were consistent with changes in levels of reactive oxygen species and malondialdehyde (MDA). The beneficial effects of ABA and CaCl₂ in ameliorating salt stress may be attributed to the reduction of membrane peroxidation and increased glutathione (GSH) levels. These observations suggest that oxidative stress resulting from salt stress in B. nigra may result in production of antioxidative enzymes to counteract oxidative damage, and the enzymes may contribute to the ability of B. nigra to survive adverse conditions. Data indicate that hormone and ion in the order of kinetin > ABA > calcium alleviate the adverse impact of salt on B. nigra.     

Quantitative and structural analyses of hazardous elements in Chinese medicines and herbs

Thirty samples of Chinese medicines and herbs were analyzed using instrumental neutron activation analysis (INAA) and X-ray diffraction (XRD) methods, mainly noting on the hazardous elements arsenic (As), mercury (Hg), chromium, antimony and cobalt. The three Niuhuang Jiedu Pian samples contained 8.6%, 8.3% and 2.2% As. Two out of four Liushen Wan samples contained approximately7% of both As and Hg. Despite being identically named, the other two Liushen Wan samples did not contain such high concentrations. Japanese Liushen Wan for children contained 1.2 ± 0.03% As and 31 ± 12 mg/kg Hg, whereas Liushen Wan for adults manufactured by another Japanese company contained 550 ± 22 mg/kg As and 1.2 ± 0.05 mg/kg Hg. All the chemical structural formulas of As and Hg in the high-concentration Niuhuang Jiedu Pian and Liushen Wan were realgar (As₄S₄), uzonite (As₄S₅) and cinnabar (HgS). Although the human body is generally not believed to absorb sulphides, continuous intake of these Chinese medicines is potentially no good because it is possible that some arsenic-sulfides will dissolve in gastric acid and then alter their chemical structures. Additionally, many herbs contained low concentrations of Hg, and their chemical structures were unknown.     

Low concentration of HgCl2 drives rat hepatocytes to autophagy/apoptosis/necroptosis in a time-dependent manner

Mercury (Hg) is known to produce hepatotoxicity driving cells towards apoptosis. It was recently reported that low concentrations of Hg (5 μM) initiate autophagy in vitro within 30 min of incubation modulated by several autophagy-related gene proteins, and co-regulators through ubiquitination. The present study aimed to elucidate in vitro mode of cytotoxic responses including programed cell death in 5-μM Hg-treated rat hepatocytes. Autophagy proceeded from 30 min to 4 hr mediated by crosstalk between specific regulating factors of cell-death-signaling mechanisms. It was noted that after 4-hr incubation with 5 μM HgCl₂, cells were driven towards apoptosis followed by necroptosis within 6.5 hr. Receptor-interacting serine-threonine protein 3 (RIP3) and caspase-8 played a significant role in interlinking function. The positive role of caspase-8 with RIP3 significantly triggered caspase-3 via extrinsic apoptotic pathway. A shift from apoptosis to necroptosis occurred after 6 hr via tumor necrosis factor α-RIP3-caspase-8 pathway. No alteration in caspase-3 expression and presence of high-mobility group box 1 protein in nucleus indicated absence of apoptosis and necrosis in rat hepatocytes between 6.5 and 8 hr. Data indicated that cellular homeostasis is regulated by modulating different proteins and driving hepatocytes through autophagy to apoptosis to necroptosis in a time-dependent manner.     

Effects of lead exposure on redox status,DNA and histological structures in Venus verrucosa gills and digestive gland

ABSTRACT

Lead (Pb) is one of the most toxic heavy metals that affect the physiological status of aquatic organisms. The present investigation evaluated the possible toxic effect of lead chloride (PbCl₂) on biomarkers responses, DNA damage and histological alterations in Venus verrucosa gills and digestive gland. Three concentrations of PbCl₂ (D1:1µgL^?1, D2: 10µgL^?1 and D3: 100µgL^?1) were chosen for V. verrucosa exposure during six days. At the end of the trial, it was found that Pb tended to accumulate in both gills and digestive gland in a dose-dependent manner. However, gill tissues exhibited the highest metal burden. Our results showed an increase of malondialdehyde, protein carbonyls and advanced oxidation protein product levels in both organs following PbCl₂exposure. The induction of both non-enzymatic and enzymatic antioxidant systems; as well as the decrease of the acetylcholinesterase activity and degradation of DNA structure was recorded in the gills and digestive gland. The histopathological alterations observed in gills (disruption of lamellas and cilia filaments?…) and digestive gland (lumens occlusion, necrosis and fibrosis) confirmed the aforementioned results. Our data highlighted the short-term toxicity effects of PbCl₂ on V. verrucosa and pointed out a high sensitivity of gills towards this metal.     

Effects of lead on calmodulin content,proliferation and interleukin-2 in lymphocytes of mice

The mechanism inderlying lead (Pb)-induced toxicity was presumed to involve interaction between Pb²⁺ and calcium (Ca²⁺) associated with calmodulin-dependent systems. The aim of this study was to (1) examine the hypothesis that Pb alters calmodulin content and (2) assess the effects of Pb on proliferation and interleukin-2 (IL-2) levels in lymphocytes. The influence of Pb on calmodulin content in mouse lymphocytes was assessed by western blot, while the proliferation of lymphocytes was studied using MTT test, and IL-2 level by ELISA assay. The results showed that 100?µM PbCl₂ decreased calmodulin content, phytohemagglutinin (PHA)-induced proliferation, and IL-2 levels, but a lower concentration (1?µM PbCl₂) did not appear to be effective. Evidence indicates that IL-2 levels and lymphocyte proliferation might not be calmodulin content dependent. Our data suggested that Pb²⁺-induced toxicity was likely to be complex with multiple factors involved, including calmodulin, IL-2, and proliferation of lymphocytes.     

In vitro cytotoxicity of multi-wall carbon nanotubes on human cell lines

The aim of this study was to evaluate the in vitro toxicity of two multi-wall carbon nanotubes on four different cell lines: human alveolar epithelial (A549) cells, hepatocytes (Hep 3B cells), human embryonic kidney cells, and intestinal (P407 cells) cells. The adverse effects of carbon nanoparticles were analyzed after 24 h incubation with different cell lines using the trypan blue dye exclusion method. Incubation of carbon nanotubes with different cells produced a concentration-dependent inhibition of growth of the cells. The TC₅₀ or IC₅₀ values (toxic concentration 50, i.e., concentration of particles inducing 50% cell mortality) of two nanoparticles were (1) found to be in the range 23.5–30.5 µg mL^?1, and (2) less than that of quartz (known toxic agent, 28.8–66.9 µg mL^?1), indicating the greater cytotoxic effect of carbon nanoparticles than quartz particles.     

PM_(2.5)和甲醛联合暴露致小鼠肺损伤及其分子机制的研究

我国城市当前普遍存在室外大气PM_(2.5)与室内甲醛(FA)联合污染状况,二者均被报道在单独暴露下可以导致肺损伤并诱导和诱发哮喘的急性发作,但其联合污染的具体效应,以及分子机制目前尚不清楚。为探究PM_(2.5)和/或甲醛暴露对小鼠的肺损伤及其可能的机制,分别将雄性Balb/c小鼠分为以下6组:对照组,AZD8055组,PM_(2.5)组,FA组,PM_(2.5)+FA组,PM_(2.5)+FA+AZD8055组。染毒结束后,观察肺组织病理学变化;检测肺组织氧化损伤,活性氧(reactive oxygen species,ROS),还原型谷胱甘肽(glutathione,GSH)和丙二醛(malondialdehyde,MDA)的含量,DNA损伤,DNA-蛋白质交联(DNA-protein crosslink,DPC)系数和8羟基脱氧鸟苷(8-OH-d G)的含量,以及细胞凋亡、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的含量。结果表明,当吸入气态甲醛浓度为3 mg·m-3,气道滴注PM_(2.5)浓度为2.5 mg·m L-1时,肺组织出现不同程度的支气管重塑和炎症细胞浸润。ROS显著上升,GSH显著下降,DPC、8-OH-d G以及Caspase-3都显著上升。添加AZD8055后,肺组织损伤效应更加显著。PM_(2.5)复合甲醛的暴露导致小鼠肺损伤具有协同作用,氧化应激及其下游的DNA损伤可能是甲醛联合PM_(2.5)致小鼠肺损伤的一种重要机制。     

根表铁膜的形成和添加硒对水稻吸收转运无机汞和甲基汞的影响

为了研究根表铁膜和硒对水稻吸收、转运不同形态的汞的影响,用Fe2+溶液诱导根表形成铁膜后,将水稻植株分别暴露于无机汞(Hg Cl2)、甲基汞(Me Hg Cl)、无机汞和亚硒酸钠(Hg Cl2+Na2Se O3)混合溶液、甲基汞和亚硒酸钠(Me Hg Cl+Na2Se O3)混合溶液的培养液中继续培养72 h。用DCB(dithionite-citrate-bicarbonate)提取根表铁膜,并用电感耦合等离子体质谱(ICP-MS)测定DCB溶液中Fe、Hg含量及水稻根、茎叶中Hg含量。结果表明:水稻根表铁膜对Me Hg Cl和Hg Cl2均有吸附,对Me Hg Cl的吸附作用高于Hg Cl2。根表铁膜的形成显著降低了汞暴露水稻根、茎叶中汞的含量;铁膜的形成也显著降低了Hg Cl2和Me Hg Cl从水稻根部到茎叶部分的转运效率。硒的存在可增加铁膜对Hg Cl2和Me Hg Cl的吸附,降低水稻对Hg Cl2和Me Hg Cl的吸收和转运。研究结果表明:根表铁膜和硒单独或联合作用能显著抑制水稻对无机汞和甲基汞的吸收和转运,进而可以减少汞在稻米中的蓄积。研究的开展对于提高汞污染区稻米的质量和保证粮食安全具有一定的现实意义。