Degradation of carbofuran and acetamiprid in wolfberry by dielectric barrier discharge plasma: Kinetics, pathways, toxicity and molecular dynamics simulation.

Carbofuran and acetamiprid pose the highest residual risk among pesticides found in wolfberries. This study aimed to degrade these pesticides in wolfberries using a multi-array dielectric barrier discharge plasma (DBD), evaluate the impact on safety and quality and explore their degradation mechanism. The results showed that DBD treatment achieved 90.6% and 80.9% degradation rates for carbofuran and acetamiprid, respectively, following a first-order kinetic reaction. The 120 s treatment successfully reduced pesticide contamination to levels below maximum residue limits. Treatment up to 180 s did not adversely affect the quality of wolfberries. QTOF/MS identification and degradation pathway analysis revealed that DBD broke down the furan ring and carbamate group of carbofuran, while replacing the chlorine atom and oxidizing the side chain of acetamiprid, leading to degradation. The toxicological evaluation showed that the degradation products were less toxic than undegraded pesticides. Molecular dynamics simulations revealed the reactive oxygen species (ROS) facilitated the degradation of pesticides through dehydrogenation and radical addition reactions. ROS type and dosage significantly affected the breakage of chemical bonds associated with toxicity (C4-O5 and C2-Cl1). These findings deepen insights into the plasma chemical degradation of pesticides.

Effects of the Pesticide Carbofuran on Two Species of Chlorophyceae (Desmodesmus communis and Pseudopediastrum boryanum) and Their Pesticide Bioremediation Ability.

Carbofuran is one of the most toxic broad-spectrum pesticides. We evaluated the effects of carbofuran on two species of microalgae, Pseudopediastrum boryanum and Desmodesmus communis, through measurements of cell viability, biomass, chlorophyll content, and the production of reactive oxygen species (ROS). The ability of these algae to remove carbofuran dissolved in the media was also determined. For the evaluations, both microalgae species were exposed to carbofuran (FURADAN 350 SC®) at concentrations of 100, 1000, and 10,000 µg L-1 for 7 days. Algae cell viability and chlorophyll-a concentration were not affected by the presence of carbofuran. Both species grew when exposed to the pesticide; however, the microalgae D. communis grew less than its respective control when exposed to the highest concentration (10,000 µg L-1 of carbofuran), indicating an adverse effect of the pesticide on this species. A significant increase in ROS production was observed in D. communis and P. boryanum when exposed to the highest concentration tested. The microalgae P. boryanum completely removed carbofuran in the media within 2 days, regardless of the concentration, whereas D. communis achieved the same result only after 5 days of exposure. Growth inhibition was observed only until the disappearance of carbofuran from the media. The present study suggests the use of microalgae, mainly P. boryanum, as potential tools for the remediation of environments contaminated by carbofuran because of their resistance to the insecticide and their ability to remove it rapidly from water. Environ Toxicol Chem 2024;43:926-937. © 2023 SETAC.

Sublethal toxicity of carbofuran in cattle egret (Bubulcus ibis coromandus): hematological, biochemical, and histopathological alterations / Toxicidade subletal do carbofurano na garça-vaqueira (Bubulcus ibis coromandus): alterações hematológicas, bioquímicas e histopatológicas

Abstract This study was aimed to investigate Carbofuran (CF)-induced pathological changes in cattle egret. Two hundred cattle egrets were reared and equally divided into four groups and given different CF concentrations (0.03 mg/L, 0.02 mg/L, 0.01 mg/L and 0 mg/L (control group)). Hematology, serum biochemistry, histopathology, and immunological markers were studied. Our results confirm that CF induces anemic conditions, leukocytosis, elevated liver enzymatic activity, and alterations in renal biomarkers. Moreover, specific microscopic lesions such as multifocal necrosis, pyknotic nuclei, hemorrhages, congestion, and inflammatory cell proliferation were observed in the liver, kidney, spleen, and thymus. These findings suggest that CF can induce harmful effects, so the application of this pesticide in the field must be strictly monitored to mitigate the possibility of exposure to non-target species.

Resumo Este estudo teve como objetivo investigar as alterações patológicas induzidas por carbofurano (CF) em garças-vaqueiras. Duzentas dessas garças foram criadas e divididas igualmente em quatro grupos e receberam diferentes concentrações de CF: 0,03 mg/L; 0,02 mg/L; 0,01 mg/L; e 0 mg/L (grupo controle). Foram realizadas análises de hematologia, bioquímica sérica, histopatologia e marcadores imunológicos. Nossos resultados confirmaram que CF induz condições anêmicas, leucocitose, atividade enzimática hepática elevada e alterações nos biomarcadores renais. Além disso, lesões microscópicas específicas, como necrose multifocal, núcleos picnóticos, hemorragias, congestão e proliferação de células inflamatórias, foram observadas no fígado, rim, baço e timo. Esses achados sugerem que o CF pode causar efeitos nocivos, portanto a aplicação desse agrotóxico no campo deve ser rigorosamente monitorada para mitigar a possibilidade de exposição a espécies não alvo.

The adsorption effects of biochar on carbofuran in water and the mixture toxicity of biochar-carbofuran in rats.

Carbofuran, a widely used carbamate insecticide, is frequently detected in water. In this study, a high-performance adsorbent (WAB4) for carbofuran was obtained from laboratory-synthesized biochars. The maximum adsorption of carbofuran by WAB4 reaches 113.7 mg/g approximately. The adsorption of carbofuran by biochar was a multi-molecular layer and the adsorption process conforms to the pseudo-second-order kinetic model (R2 = 0.9984) and Freundlich isotherm model (R2 = 0.99). Importantly, an in vivo rat model was used to assess the combined toxicological effects of biochar-carbofuran complexes. The toxicity of the complexes (LD50 > 12 mg/kg) is lower than that of carbofuran (LD50 = 7.9 mg/kg) alone. The damage of biochar-carbofuran complex on rat liver and lung is significantly less than that of carbofuran. The Cmax and bioavailability of carbofuran were found to be reduced by 64% and 68%, respectively, when biochar was present, by UPLC-MS/MS analysis of carbofuran in rat plasma. Furthermore, it was confirmed that the biochar-carbofuran complex is relatively stable in the gastrointestinal tract, by performing a carbofuran release assay in artificial gastrointestinal fluids in vitro. Collectively, biochar is a bio-friendly material for the removal of carbofuran from water.

Inter-species differences between humans and other mammals in the in vitro metabolism of carbofuran and the role of human CYP enzymes.

This study investigated the metabolic transformation of carbofuran in seven species of mammals using LC-MS/MS and liver microsomes. The results revealed species-specific differences in metabolite formation, indicating the potential role of metabolic pathways in toxicity and risk assessment. The majority of carbofuran was metabolized through the 3-hydroxycarbofuran pathway, with the highest levels observed in dogLM and the lowest in humanLM. Further analysis was conducted to investigate the human cytochrome P450-mediated metabolism of carbofuran, with CYP3A4 being found to be the most efficient enzyme with the highest contribution to the 3-hydroxycarbofuran pathway. Inhibition of CYP3A4 with ketoconazole resulted in a substantial decrease in carbofuran metabolism. In addition, carbofuran exhibited inhibitory effects on human CYP3A4 and CYP2B6, demonstrating the potential for carbofuran to interact with these enzymes. The findings highlight the importance of in vitro screening for metabolic processes and provide insights into the biotransformation of carbofuran.

Carbofuran pesticide toxicity to the eye.

Pesticide exposure to eyes is a major source of ocular morbidities in adults and children all over the world. Carbofuran (CF), N-methyl carbamate, pesticide is most widely used as an insecticide, nematicide, and acaricide in agriculture, forestry, and gardening. Contact or ingestion of carbofuran causes high morbidity and mortality in humans and pets. Pesticides are absorbed in the eye faster than other organs of the body and damage ocular tissues very quickly. Carbofuran exposure to eye causes blurred vision, pain, loss of coordination, anti-cholinesterase activities, weakness, sweating, nausea and vomiting, abdominal pain, endocrine, reproductive, and cytotoxic effects in humans depending on amount and duration of exposure. Pesticide exposure to eye injures cornea, conjunctiva, lens, retina, and optic nerve and leads to abnormal ocular movement and vision impairment. Additionally, anticholinesterase pesticides like carbofuran are known to cause salivation, lacrimation, urination, and defecation (SLUD). Carbofuran and its two major metabolites (3-hydroxycarbofuran and 3-ketocarbofuran) are reversible inhibitors of acetylcholinesterase (AChE) which regulates acetylcholine (ACh), a neurohumoral chemical that plays an important role in corneal wound healing. The corneal epithelium contains high levels of ACh whose accumulation by AChE inhibition after CF exposure overstimulates muscarinic ACh receptors (mAChRs) and nicotinic ACh receptors (nAChRs). Hyper stimulation of mAChRs in the eye causes miosis (excessive constriction of the pupil), dacryorrhea (excessive flow of tears), or chromodacryorrhea (red tears). Recent studies reported alteration of autophagy mechanism in human cornea in vitro and ex vivo post carbofuran exposure. This review describes carbofuran toxicity to the eye with special emphasis on corneal morbidities and blindness.

Transgenerational effects of co-exposure to cadmium and carbofuran on zebrafish based on biochemical and transcriptomic analyses.

The combined toxicity of heavy metals and pesticides to aquatic organisms is still largely unexplored. In this study, we investigated the combined impacts of cadmium (Cd) and carbofuran (CAR) on female zebrafish (F0 generation) and their following F1 generation. Results showed that mixtures of Cd and CAR induced acute synergistic effects on both zebrafish adults of the F0 generation and embryos of the F1 generation. Combined exposure to Cd and CAR could obviously alter the hepatic VTG level of females, and the individual exposures increased the relative mRNA levels of vtg1 and vtg2. Through maternal transmission, co-exposure of Cd and CAR caused toxicity to 4-day-old larvae of the F1 generation, evidenced by the significant changes in T4 and VTG levels, CYP450 activity, and the relative transcriptional levels of genes related to the hormone, oxidative stress, and apoptosis. These effects were also reflected by the global gene expression pattern to 7-day-old larvae of F1 generation using the transcriptomic analysis, and they could also affect energy metabolism. Our results provided a more comprehensive insight into the transgenerational toxic impacts of heavy metal and pesticide mixtures. These findings highlighted that it was highly necessary to consider transgenerational exposures in the ecological risk assessment of chemical mixtures.

Sublethal toxicity of carbofuran in cattle egret (Bubulcus ibis coromandus): hematological, biochemical, and histopathological alterations.

This study was aimed to investigate Carbofuran (CF)-induced pathological changes in cattle egret. Two hundred cattle egrets were reared and equally divided into four groups and given different CF concentrations (0.03 mg/L, 0.02 mg/L, 0.01 mg/L and 0 mg/L (control group)). Hematology, serum biochemistry, histopathology, and immunological markers were studied. Our results confirm that CF induces anemic conditions, leukocytosis, elevated liver enzymatic activity, and alterations in renal biomarkers. Moreover, specific microscopic lesions such as multifocal necrosis, pyknotic nuclei, hemorrhages, congestion, and inflammatory cell proliferation were observed in the liver, kidney, spleen, and thymus. These findings suggest that CF can induce harmful effects, so the application of this pesticide in the field must be strictly monitored to mitigate the possibility of exposure to non-target species.

Assessment of reproductive toxicity of carbofuran and copper sulfate in male Nile tilapia (Oreochromis niloticus).

This study's hypothesis is that carbofuran and copper sulfate have a synergistic harmful impact on the fertility of male Nile tilapia. Hence, this study was designed to assess the toxic reproductive outcome of carbofuran, copper sulfate, and their mixture in male Nile tilapia. Sixty male Nile tilapia fishes were separated into four groups (15 fish/group). The control group; carbofuran group, was given dechlorinated tap water containing 0.02 mg/L (1/10 dose of LC50) carbofuran; copper group was given dechlorinated tap water containing 4.0 mg/L (1/10 dose of LC50) copper sulfate; carbofuran + copper sulfate group received dechlorinated tap water containing 0.02 mg/L carbofuran plus 4.0 mg/L copper sulfate. After 6 weeks, results revealed a significant rise in testicular malondialdehyde levels and a significant decrease in testicular reduced glutathione contents among all experimental groups compared to the control group. Testicular testosterone levels were significantly declined in copper and combined groups compared to the control. The seminal evaluation using computer-assisted sperm analysis showed a significant decline in the progressive motility percentage, motile ratio percentage, sperm concentration, curvilinear velocity, straight-line velocity, average path velocity, and wobble in all intoxicated groups, particularly, the combined group. The histopathology of testes in all intoxicated groups revealed a detachment of the basal membrane of some seminiferous tubules, and others were free from spermatogonia and spermatozoa with interstitial eosinophilic granular cell infiltration. Testicular lesions were more severe in the combined group. Finally, it was concluded that carbofuran and copper sulfate exerted a negative effect on the reproductive function of male Nile tilapia, and they have a synergistic harmful impact on the fertility of male Nile tilapia.

Co-exposure of carbon nanotubes with carbofuran pesticide affects metabolic rate in Palaemon pandaliformis (shrimp).

Palaemon pandalirformis (shrimp) is a species widely distributed in the Brazilian coastal region and with an important economic role. In addition, this organism is considered an indicator of environmental pollution in estuaries; however, its physiological responses to toxic environmental pollutants, including pesticides and nanomaterials, are not well known, mainly, the effects of co-exposure. Thus, the purpose of this study was to evaluate the ecotoxicological effects of co-exposure between oxidized multiwalled carbon nanotubes (HNO3-MWCNT) and carbofuran pesticide on the routine metabolism of P. pandalirformis. The shrimps were exposed to different concentrations of HNO3-MWCNT (0; 10; 100; 500; 1000 µg L-1), carbofuran (0; 0.1; 1.0; 5.0; 10 µg L-1) and to co-exposure with 100 µg L-1 of HNO3-MWCNT + carbofuran (0; 0.1; 1.0; 5.0; 10 µg L-1), to evaluate the effects on metabolic rate (O2 consumption) and excretion of ammonia (NH4+NH3). Our results showed that the shrimps exposed to HNO3-MWCNT (10 µg L-1) increased the metabolic rate by 292% and the excretion of ammonia by 275%; those exposed to carbofuran (10 µg L-1) increased their metabolic rate by 162% and the excretion of ammonia by 425%; and with the co-exposure of HNO3-MWCNT + carbofuran there was also an increase in the metabolic rate by 317% and an excretion of ammonia by 433% when compared to control. These findings provides useful information toward better understanding the physiological responses of shrimps after combined exposure to nanomaterials and pesticides in aquatic environments.

Co-Treatment of Copper Oxide Nanoparticle and Carbofuran Enhances Cardiotoxicity in Zebrafish Embryos.

The use of chemicals to boost food production increases as human consumption also increases. The insectidal, nematicidal and acaricidal chemical carbofuran (CAF), is among the highly toxic carbamate pesticide used today. Alongside, copper oxide nanoparticles (CuO) are also used as pesticides due to their broad-spectrum antimicrobial activity. The overuse of these pesticides may lead to leaching into the aquatic environments and could potentially cause adverse effects to aquatic animals. The aim of this study is to assess the effects of carbofuran and copper oxide nanoparticles into the cardiovascular system of zebrafish and unveil the mechanism behind them. We found that a combination of copper oxide nanoparticle and carbofuran increases cardiac edema in zebrafish larvae and disturbs cardiac rhythm of zebrafish. Furthermore, molecular docking data show that carbofuran inhibits acetylcholinesterase (AChE) activity in silico, thus leading to impair cardiac rhythms. Overall, our data suggest that copper oxide nanoparticle and carbofuran combinations work synergistically to enhance toxicity on the cardiovascular performance of zebrafish larvae.

Role of Citrus medica L. Fruits Extract in Combatting the Hematological and Hepatic Toxic Effects of Carbofuran.

Citrus medica L. is rich in numerous vital bioactive constituents, though it is an underutilized among the citrus genus. Therefore, the aim of the present investigation was to evaluate the protective role of the C. medica fruit (CMF) methanol extract against carbofuran (CF)-induced toxicity in experimental rats. In addition, this work aims at detecting and measuring polyphenolic compounds by means of high-performance liquid chromatography (HPLC) and evaluation of the antioxidant activity of this extract. For this, studies dealing with serum hematological and biochemical parameters, liver endogenous antioxidants, as well as hepatic histo-architectural features have been carried out to assess the protective ability of CMF against CF-induced toxicity. Additionally, total phenol, flavonoid, and antioxidant capability were measured and the antioxidant action was investigated using DPPH and nitric oxide radical scavenging assays as well as reducing power assessments. HPLC results revealed the presence of benzoic acid, cinnamic acid, gallic acid, quercetin, and salicylic acid in CMF extract. Furthermore, results showed that CMF has considerable total phenol, flavonoid, and antioxidant capability and exhibits significant free radical scavenging and reducing potentialities. On the other hand, CF intoxication of rats significantly altered the hematological and serum biochemical parameters with hepatocytes disruption. Carbofuran also caused an upsurge in malondialdehyde (MDA) level and a decline in hepatic cellular antioxidant enzymes levels in rats compared to the control group. Co-administration of CMF amended the anomalies and improved the histo-architectural arrangement of hepatocytes in treated groups. CMF also inhibited the alteration of endogenous antioxidant enzymes and MDA levels as compared to the carbofuran treated group and returned them to their normal state. Taken all together, results from this investigation highlight the protective role of CMF against CF-induced toxicity which might be attributed to the polyphenolic constituents of the extract.

Severe carbamates intoxication of 43-year-old farmer - case report.

INTRODUCTION: Carbamate insecticides are methyl carbamic acid esters and reversible cholinesterase inhibitors. In contrast to the long-term action of organophosphate insecticides, this complex undergoes rapid hydrolysis. CASE REPORT: A suicidal poisoning by exposure to carbofuran in a 43-year-old farmer is reported. The patient had a sudden respiratory and cardiac arrest in the mechanism of bradycardia asystole. He was additionally diagnosed with metabolic acidosis and massive aspiration pneumonia. After applied treatment, the patient's general condition improved - alignment of efficiency of both respiratory and circulatory efficiency were reached. CONCLUSION: Carbofuran is one of the most toxic carbamate insecticides. It is therefore important to react quickly and choose the right treatment. Differentiation between organophosphate and carbamate intoxication is essential.

Carbofuran cytotoxicity, DNA damage, oxidative stress, and cell death in human umbilical vein endothelial cells: Evidence of vascular toxicity.

Carbofuran is a broad-spectrum carbamate insecticide, which principally inhibits the acetylcholinesterase (AChE) enzyme in the nervous system. Nonetheless, their selective action is not restricted to a single species and expanded to humans. No studies are available on the toxicological effects of carbofuran in the endothelial cells (ECs), which first confronts the toxicants in blood vessels. Hence, we have exposed the human umbilical vein ECs (HUVECs) with carbofuran for 24 h, which significantly reduced the cell survival to 25.16% and 33.48% at 500 and 1,000 µM analyzed by MTT assay. In the neutral red uptake (NRU) assay, 16.68%, 30.99%, and 58.11% survival decline was found at 250, 500, and 1,000 µM of carbofuran. HUVECs exposed to carbofuran showed significant increase in the intracellular reactive oxygen species (ROS), indicating oxidative stress at low concentrations. In parallel, HUVECs showed hyperpolarization effects in the mitochondrial membrane potential (ΔΨm) upon carbofuran exposure. Carbofuran induced DNA damage in HUVECs measured as 8.80, 11.82, 35.56, and 79.69 Olive tail moment (OTM) in 100-, 250-, 500-, and 1,000-µM exposure groups. Flow cytometric analysis showed apoptotic peak (SubG1) and G2M arrest in the HUVECs exposed to carbofuran. Overall, our novel data confirm that carbofuran is toxic for the EC cells, especially at the higher concentrations, which may affect the vascular functions and possibly angiogenesis. Hence, carbofuran should be applied judiciously, and detailed vascular studies are warranted to gain an in-depth information focusing the transcriptomic and translation changes employing suitable in vivo and in vitro test models.

Effect of kebar grass extract ( Biophytum petersianum Klotzsch) on histopathological changes in liver of mice offspring from the parent exposed to carbofuran during lactation period.

This study aims to determine the potential of Kebar grass extract in reducing the impact of liver damage in mice offspring ( Mus musculus) from parent exposed to carbofuran during lactation period. 42 lactation mice ( Mus musculus) used in the study were divided into seven groups, each group consisting of six mice. Carbofuran, Kebar grass extract, and vitamin C are administered orally on days 1 to 14 after birth. This group consisted of K (aquadest), P1 (carbofuran 1/4 LD50 0.0125 mg/day), P2 (carbofuran 1/8 LD50 0.00625 mg/day), P3 (Kebar grass extract 3.375 mg (0.2 ml) + carbofuran 1/4 LD50), P4 (Kebar grass extract 3.375 mg (0.2 ml) + carbofuran 1/8 LD50), P5 (vitamin C 5 mg (0.2 ml) + carbofuran 1/4 LD50), and P6 (vitamin C 5 mg (0.2 ml) + carbofuran 1/8 LD50). On the 15th day after birth, mice were sacrified and their liver taken for microscopic examination with hematoxilin and eosin staining. The scoring data were analyzed using Kruskal-Wallis and Mann-Whitney test. The result showed significant different (p⟨0.05) among the treatment groups. Mean of P4 in degeration is (1.13), necrosis (1.13) and inflamation (0.73), while the mean of P6 in degeneration is (2.20), necrosis (2.73) and inflamation (1.93). The conclusion of this research is giving Kebar grass extract is more effective in reducing degeneration, necrosis and inflammatory cell's infiltration than vitamin C in in mice offspring ( Mus musculus) from parent exposed to carbofuran during lactation period.

Effect of allicin on antioxidant defense system, and immune response after carbofuran exposure in Nile tilapia, Oreochromis niloticus.

In this work, allicin was evaluated as an immunostimulant and antioxidant agent preventing Nile tilapia; Oreochromis niloticus against carbofuran toxicity. Fish (60 ± 8 g) were allocated to five groups; the first group (control), the second group was fed 1 g/kg allicin-supplemented diets without carbofuran intoxication, the third group exposed to 1/10 LC50 carbofuran (0.246 mg/L). While the fourth, and fifth groups were fed allicin supplemented diet at concentration of 0.5 and 1 g/kg diet, respectively, and exposed to carbofuran at the same concentration similar to the one of the third group. After 30 days, fish exposed to carbofuran showed high ALT, AST, ALP, cholesterol, glucose, cortisol, uric acid, and creatinine levels. However, serum AChE, total proteins, immunoglobulins, and lysozyme activity were markedly (P ≤ 0.05) reduced in carbofuran exposed tilapia fish. Moreover, malondialdehyde (MDA) level was significantly increased in liver, and kidneys tissues of carbofuran exposed fish. Whereas, catalase (CAT) activity, superoxide dismutase (SOD), and total antioxidant capacity (TAC) were decreased (P ≤ 0.05) significantly in both liver, and kidneys tissues after exposure to carbofuran. Interestingly, tilapia fish treated with carbofuran (0.246 mg/L) and fed (0.5 and 1 g/kg diet) allicin in both the 4th & 5th groups, respectively, decreased serum biochemical parameters; and hepatorenal (MDA) levels, as well as increased AChE, immunological profile, and oxidative stress biomarkers. The results suggested that co- administration of allicin at the high dose is more capable of improving the biochemical, and immunological parameters, and tissue antioxidant responses of carbofuran treated fish.

Simultaneous degradation of triazophos, methamidophos and carbofuran pesticides in wastewater using an Enterobacter bacterial bioreactor and analysis of toxicity and biosafety.

Triazophos (TAP), methamidophos (MAP) and carbofuran (CF) pesticides are highly toxic, soluble and absorbable. Efficient co-degradation of multi-pesticides is rare reported. The objectives of this study were to investigate TAP, MAP and CF co-degradative ability of Enterobacter sp. Z1 and study the degradation mechanisms. Strain Z1 was shown to efficiently co-degrade TAP, MAP and CF when they were used as primary carbon sources. The degradation occurred over a wide range of temperatures, pH values and pesticide concentrations and followed first-order kinetics. Under the optimum conditions (37 °C, pH 7 and 100 mg/L of each pesticide), the degradation efficiencies were 100%, 100%, and 95.3% for TAP, MAP and CF, respectively. In addition, strain Z1 could simultaneously degrade TAP, MAP, CF and total nitrogen in wastewater in a batch bioreactor, with high removal efficiencies of 98.3%, 100%, 98.7% and 100%, respectively. Genomics, proteomics, qRT-PCR and gene overexpression analyses revealed that the degradation mechanisms involved the activities of multiple proteins, among which, organophosphorus hydrolase (Oph) and 3-hydroxyacyl-CoA dehydrogenase (PaaC) are primarily responsible for TAP and MAP degradation, while carbofuran hydrolase (Mcd) and amidohydrolase (RamA) primarily degrade CF. Among these enzymes, PaaC and RamA are newly identified pesticide-degrading enzymes. Toxicity assays of strain Z1 using reporter recombinase gene (recA) and zebrafish showed that there was no accumulation of toxic metabolites during the degradation process. Biosafety test using zebrafish showed that the strain was nontoxic toward zebrafish. Strain Z1 provides a good purification effect for pesticides-containing wastewater and novel microbial pesticide-degrading mechanisms were discovered.

Individual and mixture toxicity of carbofuran and diuron to the protozoan Paramecium caudatum and the cladoceran Ceriodaphnia silvestrii.

The toxicity of the insecticide carbofuran and herbicide diuron (individually and in mixture) to the invertebrates Paramecium caudatum and Ceriodaphnia silvestrii was evaluated. Acute and chronic toxicity tests were carried out with the diuron and carbofuran active ingredients and their commercial products, Diuron Nortox® 500 SC and Furadan® 350 SC, respectively. Individual toxicity tests showed that C. silvestrii was more sensitive to both carbofuran and diuron than P. caudatum. In single exposures, both pesticides caused adverse effects to C. silvestrii in environmentally relevant concentrations (48 h EC50 = 0.001 mg L-1 and 8 d LOEC = 0.00038 mg L-1 for formulated carbofuran; 8 d LOEC < 0.05 mg L-1 for formulated diuron). For P. caudatum, carbofuran and diuron in single exposures were only slightly toxic (24 h IC50 = 5.1 mg L-1 and 6.9 mg L-1 for formulated carbofuran and diuron, respectively). Acute and chronic exposures to diuron and carbofuran mixtures caused significant deviations of the toxicity predicted by the Concentration Addition and Independent Action reference models for both test species. For the protozoan P. caudatum, a dose-dependent deviation was verified for mortality, with synergism caused mainly by carbofuran and antagonism caused mainly by diuron. For protozoan population growth, however, an antagonistic deviation was observed when the active ingredient mixtures were tested. In the case of C. silvestrii, antagonism at low concentrations and synergism at high concentrations were revealed after acute exposure to active ingredient mixtures, whereas for reproduction an antagonistic deviation was found. Commercial formulation mixtures presented significantly higher toxicity than the active ingredient mixtures. Our results showed that carbofuran and diuron interact and cause different toxic responses than those predicted by the individually tested compounds. Their mixture toxicity should therefore be considered in risk assessments as these pesticides are likely to be present simultaneously in edge-of-field waterbodies.

Carbofuran toxicity and its microbial degradation in contaminated environments.

Carbofuran is one of the most toxic broad-spectrum and systemic N-methyl carbamate pesticide, which is extensively applied as insecticide, nematicide and acaricide for agricultural, domestic and industrial purposes. It is extremely lethal to mammals, birds, fish and wildlife due to its anticholinesterase activity, which inhibits acetyl-cholinesterase and butyrylcholinesterse activity. In humans, carbofuran is associated with endocrine disrupting activity, reproductive disorders, cytotoxic and genotoxic abnormalities. Therefore, cleanup of carbofuran-contaminated environments is of utmost concern and urgently needs an adequate, advanced and effective remedial technology. Microbial technology (bacterial, fugal and algal species) is a very potent, pragmatic and ecofriendly approach for the removal of carbofuran. Microbial enzymes and their catabolic genes exhibit an exceptional potential for bioremediation strategies. To understand the specific mechanism of carbofuran degradation and involvement of carbofuran hydrolase enzymes and genes, highly efficient genomic approaches are required to provide reliable information and unfold metabolic pathways. This review briefly discusses the carbofuran toxicity and its toxicological impact into the environment, in-depth understanding of carbofuran degradation mechanism with microbial strains, metabolic pathways, molecular mechanisms and genetic basis involved in degradation.

Mechanism insights into the transformation of carbosulfan during apple drying processes.

The transformation of carbosulfan (CSN) in apples was investigated during oven-drying, microwave drying, and sun-drying. CSN transformed primarily into carbofuran (COA) during these drying processes. The conversion kinetics of CSN and COA was fitted by curve regression and mainly conformed to quadratic models (R2 = 0.70-0.97). Oven-drying promoted the transformation of CSN into COA. Microwave drying resulted in the highest scavenging capacity against CSN and COA (41%-100%). Moreover, a transformation mechanism was proposed on the basis of density functional theory (DFT) calculation. The COA originated from a series of chemical reactions involving hydroxyl substitution, cleavage, and oxidation; this result was further confirmed on the basis of molecular electrostatic potential (MEP) and molecular orbital theory. Furthermore, the toxicity and stability of CSN and COA were evaluated with the T.E.S.T. program. COA was less toxic than CSN to aquatic organisms but more toxic than CSN to rats. Therefore, COA production should be avoided during drying. Microwave drying was found to be the optimum choice for drying apples.