The use of calcium carbide in food and fruit ripening: Potential mechanisms of toxicity to humans and future prospects.

The global increase in the demand for ripe fruits has induced unhealthy use of toxic chemicals in fruit ripening. One of such chemicals in common use is calcium carbide (CaC2). Due to its nature, commercial CaC2 is consistently found to contain impurities such as Arsenic and other toxic and carcinogenic chemicals. Few studies have only reported acute associative effects of CaC2, whereas there is only sparse evidence of its chronic and long-term impact. This article reviewed all the information on the nature of commercial CaC2 used for food processing. Meanwhile, all reports on the acute effects of CaC2, such as skin burns, skin irritations and inflammation, were summarized. Despite reported acute cases, an increase in commercial CaC2 for fruit ripening has been reported in recent times, especially in developing countries, as many vendors may consider the toxic effects/risks as negligible. Therefore, this study highlighted the paucity in research studies on the chronic impact of commercial CaC2 while proposing possible mechanisms for CaC2 induction of cancer, cardiovascular dysfunction, diabetic mellitus and others. Furthermore, suggestions on further studies to unravel the chronic impacts of CaC2 on health and recommendations for viable alternatives of fruit ripening with minimal or zero toxicity were proffered. Finally, other suggestions such as improving CaC2 detection technologies and innovative grassroots educational programs will strengthen national and international agencies to enforce restrictions on the illicit use of the toxicant for fruit ripening.

Modulatory activities of polyphenols on crude acetylene-induced cardiac and hepatic dysfunctions in a rat model.

Exposure to crude acetylene can occur in occupational settings. This study assessed the modulatory activities of selected polyphenols on the hematotoxic, cardiotoxic, and hepatotoxic effects of crude acetylene. Wistar rats were exposed to 58 000 ppm crude acetylene for 10 min at 12 h intervals for 30 days. Some exposed groups were treated with 50 mg/kg rutin, quercetin, gallic acid, or tannic acid. Indices of hematological disorder, oxidative stress, and cardiovascular and hepatocellular injuries were evaluated in animals. The results showed a decrease in the levels of hematological indices in crude acetylene-exposed animals except for white blood cell count which was increased. Decreased activity/level of reduced glutathione, superoxide dismutase and ferric reducing antioxidant power with increased lipid peroxidation was observed in animals exposed to crude acetylene. Activities of transaminases, γ-glutamyl transpeptidase, and level of bilirubin were increased while the plasma albumin level was decreased. Dyslipidemia, increased activities of lactate dehydrogenase and creatine kinase-MB, and severe histopathological damage to hepatic and cardiac tissues were also observed in animals exposed to the gas. These deleterious hematological, biochemical, and histopathological changes were ameliorated in crude acetylene-toxified rats treated with the polyphenols. Tannic acid exhibited better activity than gallic acid while quercetin showed a superior activity to rutin. The results indicate that exposure to crude acetylene can lead to blood, heart, and liver-related diseases and dietary polyphenols could provide protective benefits.

Exposure of calcium carbide induces apoptosis in mammalian fibroblast L929 cells.

Inspite of various health warnings from Government and health organizations, Calcium carbide (CaC2) is still the most commonly and widely used artificial fruit ripener, probably due to its easy availability, low cost and convenience of usage. Assessment of the hazardous effects of the CaC2 applications for fruit ripening has been a matter of interest since long. Several in vivo studies have reported the toxicological outcomes such as histopathological changes in lungs and kidneys, haematological and immunological responses, upon exposure with CaC2. However, a well-controlled study investigating the effects of CaC2 under in-vitro setup was lacking. Hence, this study has been conducted to explore the toxicity associated cellular events in L929 cells exposed with varying concentrations of CaC2 (0.00312-0.2 µg/µl) for 24 h exposure time. A 23.14% reduction in cell viability was observed at the highest dose of CaC2. A similar trend in cellular stress levels at 0.2 µg/µl dose was observed in terms of rounded cellular morphology and decreased adherence as compared to the control. Furthermore, Annexin V FITC/PI staining and subsequent confocal imaging revealed a similar trend of CaC2 induced apoptosis in a dose dependent manner. A gradual elevation of intracellular ROS has also been observed up to 0.025 µg/µl dose. Thus, the study concludes that short term CaC2 exposure may increase the cellular oxidative stress and disturb the redox balance of the cell which then undergoes apoptosis. The study concludes that the exposure of CaC2 can be associated with severe diseases and suggests to stop the uses of CaC2 as fruit ripening agent.

Acute and subacute toxicity evaluation of calcium carbide and ethylene glycol in Wistar albino rats.

Background Naturally ripened fruits play a vital role in human nutrition. Under certain conditions, synthetic chemicals like calcium carbide (CaC2) and ethylene glycol (EG) are being freely used illegally in India and other countries for fruit ripening without serious concern on its toxic effects. This preclinical study evaluated the toxicity on different organs after the exposure of industrial-grade CaC2 and EG to the rats. Methods Acute toxicity was induced by the oral administration of a single dose of chemicals to the rats, and their morbidity and mortality were monitored. For subacute study, different organs of animals were analyzed biochemically and histologically after the exposure of low doses of chemicals for 30 days. Results At an acute dose of 5 mg/kg body weight of CaC2, 85% of the animals were found dead within 14 days; however, no mortality was observed following EG administration. At subacute doses, RBC and hemoglobin levels were found to be declined (p < 0.01), whereas total WBC and platelet counts, especially lymphocytes, were elevated remarkably (p < 0.01). Total protein, albumin, and urea were also found to be increased (p < 0.01). Histopathological observations support the toxicity in rats at higher doses of CaC2 and EG. Conclusions The study revealed that the artificial fruit-ripening agents like CaC2 and EG cause toxic effects on the internal organs of rats. The subsequent inflammatory response might have weakened the immune system. This in turn suggests the requisite for urgent measures to regulate the use of harmful synthetic agents in fruit ripening.

Room saturation with acetylene: a new and lethal manner of theft. A medico-legal case.

In pathological-forensic literature blast injuries are usually studied in relation to suicides, homicides during terroristic attacks and accidental events on the workplace, while the finding of these kinds of fatalities during misdoing is a recent occurrence. The Authors describe the peculiar case of the accidental death of the member of a criminal mob specialized in thefts to ATMs using acetylene tanks. The victim, having poured out the acetylene with the intent of triggering an explosion, was involved in the blast of the tank, deceasing immediately. This unusual manner of death highlights the danger of room saturation with acetylene, a criminal technique becoming more and more popular in the last years.

Modifications of carbon black nanoparticle surfaces modulate type II pneumocyte homoeostasis.

Inhalation uptake of carbon black nanoparticles (CBNP) bears the risk of morphological and functional lung impairment attributed to the highly reactive particle surface area. Chemical particle surface modifications might affect particle-cell interactions; however, thus far these alterations have not been determined. This is the first in vivo study comparing particle-induced acute lung injury using Printex(®)90 (Pr90, 7 µg), Printex®90 covered by benzo[a]pyrene or 9-nitroanthracene (BaP-Pr90, NA-Pr90, 7 µg, 15% BaP or NA by weight), and acetylene carbon black (CB) with polycyclic aromatic hydrocarbons (PAH-AB, 7 µg, 20% PAH by weight). All particles were suspended in distilled water with bovine serum albumin (BSA). In addition, the influence of suspension media was tested using Printex®90 suspended without BSA (Pr90(-BSA), 7 µg). Quartz (DQ12, 7 µg), 70 µl saline (NaCl), and distilled water with or without BSA (H2O(+/-BSA)) were used as reference and controls. It was postulated that CBNP surface modifications trigger pulmonary responses. After oropharyngeal particle aspiration, lung functions were measured 2 d postexposure, followed by lung preparation for histological or bronchoalveolar lavage fluid (BALF) examinations and type II pneumocyte isolation on d 3. Head-out body plethysmography revealed reduced flow rates induced by PAH-AB. Examinations of BALF demonstrated reduced influx of macrophages after exposure to Pr90(-BSA) and decreased lymphocyte levels after Pr90(+BSA) or BaP-Pr90 treatment. Further, CBNP induced changes in mRNA expressions (surfactant proteins) in type II pneumocytes. These findings indicate that CBNP surface area and media modulate interactions between NP and lung cells in short-term experiments.

Evaluation of the toxic potential of calcium carbide in the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ)Bg(9).

In the present study the toxic potential of calcium carbide (CaC2) was studied on the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ)Bg(9). The third instar larvae were exposed to 2, 4, 8, 16 and 32×10(-3)g/ml of CaC2 in diet for 24h. The results reveal that the dose 2×10(-3)g/ml was not toxic but the remaining doses showed a dose dependent significant increase in the hsp70 expression, ß-galactosidase activity, tissue damage, oxidative stress markers (lipid peroxidation and protein carbonyl content), glutathione-S-transferase activity, expression of Caspase 3 and 9, apoptotic index and DNA damage (midgut cells). A significant reduction as compared to control group in total protein, glutathione content and acetylcholinesterase activity was also observed. The Inductively Coupled Plasma Atomic Emission Spectroscopy analysis (ICPAES) reveals the presence of copper, iron, sodium, aluminium, manganese, calcium, nickel and mercury. The toxic effects of CaC2 in the present study may be attributed to the impurities present in it.

Interstitial pneumonitis after acetylene welding: a case report.

Acetylene is a colorless gas commonly used for welding. It acts mainly as a simple asphyxiant. In this paper, however, we present a patient who developed a severe interstitial pneumonitis after acetylene exposure during aluminum welding. A 44-year old man was welding with acetylene, argon and aluminum electrode sticks in a non-ventilated aluminum tank for 2 h. Four hours after welding dyspnea appeared and 22 h later he was admitted at the Emergency Department due to severe respiratory insufficiency with pO2 = 6.7 kPa. Chest X-ray showed diffuse interstitial infiltration. Pulmonary function and gas diffusion tests revealed a severe restriction (55% of predictive volume) and impaired diffusion capacity (47% of predicted capacity). Toxic interstitial pneumonitis was diagnosed and high-dose systemic corticosteroid methylprednisolone and inhalatory corticosteroid fluticasone therapy was started. Computed Tomography (CT) of the lungs showed a diffuse patchy ground-glass opacity with no signs of small airway disease associated with interstitial pneumonitis. Corticosteroid therapy was continued for the next 8 weeks gradually reducing the doses. The patient's follow-up did not show any deterioration of respiratory function. In conclusion, acetylene welding might result in severe toxic interstitial pneumonitis that improves after an early systemic and inhalatory corticosteroid therapy.

Fatal carbon monoxide intoxication after acetylene gas welding of pipes.

Acetylene gas welding of district heating pipes can result in exposure to high concentrations of carbon monoxide. A fatal case due to intoxication is described. Measurements of carbon monoxide revealed high levels when gas welding a pipe with closed ends. This fatality and these measurements highlight a new hazard, which must be promptly prevented.

Nematicidal activities of acetylene compounds from Coreopsis lanceolata L.

1-Phenylhepta-1,3,5-triyne (1), 5-phenyl-2-(1'-propynyl)-thiophene (2), and 2-(3'-acetoxy-1'-propynyl)-5-phenylthiophene (3) were isolated from Coreopsis lanceolata L., and their structures identified by spectroscopic methods. Compounds 1 and 2 showed effective nematicidal activities against Bursaphelenchus xylophilus and Caenorhabditis elegans, but had hardly any effect against Pratylenchus penetrans. Compound 3 did not show any effective nematicidal activity.

Isolation and structure elucidation of cytotoxic polyacetylenes and polyenes from Echinacea pallida.

Bioassay-guided fractionation of n-hexane extracts of Echinacea pallida (Asteraceae) roots led to the isolation and structure elucidation of two polyacetylenes (1, 3) and three polyenes (2, 4, 5). Two are known hydroxylated compounds, namely 8-hydroxy-pentadeca-(9E)-ene-11,13-diyn-2-one (1) and 8-hydroxy-pentadeca-(9E,13Z)-dien-11-yn-2-one (2). Two dicarbonylic constituents, namely pentadeca-(9E)-ene-11,13-diyne-2,8-dione (3) and pentadeca-(9E,13Z)-dien-11-yne-2,8-dione (4), were isolated and characterized for the first time. Furthermore, the structure elucidation of pentadeca-(8Z,13Z)-dien-11-yn-2-one (5) is described. The structure of the compounds isolated was determined on the basis of UV, IR, NMR (including 1D and 2D NMR experiments, such as 1H-1H gCOSY, gHSQC-DEPT, gHMBC, gNOESY) and MS spectroscopic data. The cytotoxic activity of the isolated constituents against MIA PaCa-2 human pancreatic adenocarcinoma cells was evaluated in the concentration range 1-100 microg/ml. Results show that the hydroxylated compounds (1, 2) have low cytotoxicity, while the more hydrophobic polyacetylenes (3) and polyenes (4, 5) displayed moderate activity.

Cometabolic transformation of cis-1,2-dichloroethylene and cis-1,2-dichloroethylene epoxide by a butane-grown mixed culture.

Aerobic cometabolism of cis-1,2-dichloroethylene (c-DCE) by a butane-grown mixed culture was evaluated in batch kinetic tests. The transformation of c-DCE resulted in the coincident generation of c-DCE epoxide. Chloride release studies showed approximately 75% oxidative dechlorination of c-DCE. Mass spectrometry confirmed the presence of a compound with mass-to-charge-fragment ratios of 112, 83, 48, and 35. These values are in agreement with the spectra of chemically synthesized c-DCE epoxide. The transformation of c-DCE required O2, was inhibited by butane and was inactivated by acetylene (a known monooxygenase inactivator), indicating that a butane monooxygenase enzyme was likely involved in the transformation of c-DCE. This study showed c-DCE epoxide was biologically transformed, likely by a butane monooxygenase enzyme. c-DCE epoxide transformation was inhibited by both acetylene and c-DCE indicating a monooxygenase enzyme was involved. The epoxide transformation was also stopped when mercuric chloride (HgCl2) was added as a biological inhibitor, further support a biological transformation. To our knowledge this is the first report of the biological transform c-DCE epoxide by a butane-grown culture.

Exploring the structural basis of neurotoxicity in C(17)-polyacetylenes isolated from water hemlock.

Water hemlock, Cicuta virosa, belonging to the Umbelliferae, is well-known as a toxic plant responsible for lethal poisonings in humans as well as animals, causing tonic and clonic convulsions and respiratory paralysis. Cicutoxin (1), being a major violent toxin of the plant, is a chemical in the class of C(17)-polyacetylenes bearing a long pi-bond conjugation system, a terminal hydroxyl, and an allylic hydroxyl in its structure, and a variety of its analogues have been isolated from the plant. In the present study, various derivatives of these toxins were synthesized through acetylation, methylation, and oxidation of cicutoxin (1) and virol A (3) and B (4). 1-Dehydroxyvirol A (28) was prepared through the coupling of (7S)-dodeca-3,5-dien-1-yn-7-ol and 1-iodopentyne under Sonogashira's conditions. A monoacetylenic compound (29) was also prepared through the coupling of (5S)-1-chlorodeca-1,3-dien-5-ol and 1-iodopentyn-5-ol. The structure-activity relationships involved in the acute toxicity of cicutoxin derivatives in mice were investigated, and the length and geometry of pi-bond conjugation and the O-functional groups were found to be important for activity. The potency in inhibition of the specific binding of the noncompetitive GABA antagonist, [(3)H]EBOB, to GABA-gated Cl(-) channels of GABA receptors in rat brain cortex was found to be correlated with acute toxicity, indicating that the ability to bind to these channels plays an important role in the acute toxicity of these compounds.

Synthesis and anticonvulsant activity of acetylenic quinazolinone derivatives.

Acetylenic derivatives of quinazolinones and quinazolinediones were synthesized and evaluated for their anticonvulsant activity. Most compounds displayed seizure-antagonizing activity in the maximal electroschock test (MES test) in most cases associated with little or no acute neurotoxicity determined in the rotorod test. Only three compounds exhibited significant activity in the seizure threshold test with subcutaneous pentylenetetrazole (scMet test). Based on the ED50 in the MES test, 1,3-bis-(prop-2-ynyl)-quinazoline-2,4-(1H,3H)-dione(9a) was about ten-fold less active than phenytoin or carbamazepine but about as active as mesuximide.

A review of the volatile metabolites of fungi found on wood substrates.

The holdings of eight collections of fungi have been examined for organisms isolated from wood and/or trees. Further selection of these fungi has been made according to their reported ability to produce volatile, biologically active metabolites. It is emphasized that the isolates in the collections do not necessarily produce such metabolites. The list of fungi fulfilling these conditions is slightly augmented by reports we have found in the literature, where the fungi concerned have not yet been deposited. The biochemistry of these compounds is considered with particular emphasis on their biosynthesis including that by Homo sapiens. The physiological and toxicological activity of these metabolites is reviewed especially with reference to their potential role in the complex symbioses existent in, for example, a tree. The review concludes with a discussion of areas of botany deserving increased attention in the hope that this will stimulate further work. The statements in the review are based on 173 references.

Dichloroacetylene: effects on the rat trigeminal nerve somatosensory evoked potential.

Humans overexposed to trichloroethylene (TCE), under specific conditions, were reported to develop trigeminal nerve dysfunction. A degradation byproduct dichloroacetylene (DCA), however, has been suggested as the probable neurotoxicant rather than TCE. Studies in mice, rats, and rabbits support the hypothesis of DCA-induced trigeminal neurotoxicity. This study, therefore, was conducted to characterize DCA-induced trigeminal nerve dysfunction in rats using the electrodiagnostic procedure trigeminal nerve-stimulated somatosensory evoked potential (TSEP). A group of six rats was exposed once to DCA (approximately 300 ppm) or room air for 2.25 h and a separate group of six rats was not exposed and served as controls. Trigeminal nerve somatosensory evoked potentials (TSEPs) were collected before exposure and 2, 4, and 7 days postexposure. Because DCA was manufactured from TCE with acetylene added as a stabilizer, another group of rats was exposed to TCE and acetylene without generation of DCA. TSEPs from DCA-exposed rats were smaller and slower compared to their baseline recordings and to the concurrent negative controls. TSEPs from the controls and the TCE/acetylene-exposed rats were unchanged. Neuropathology did not reveal treatment-related lesions. It was concluded that the rat is mildly to markedly susceptible to DCA-induced trigeminal nerve dysfunction as assessed by TSEP, but that the kidney was the likely target organ based on gross observations and the DCA literature.

Induction of poly(ADP-ribosyl)ation in the kidney after in vivo application of renal carcinogens.

Dichlorovinylcysteine, the key metabolite thought to be responsible for the nephrocarcinogenicity of trichloroethene and dichloroacetylene, induces DNA double-strand breaks followed by increased poly(ADP-ribosyl)ation of nuclear proteins in cultured renal cells (Vamvakas et al., 1992, Biochem. Pharmacol. 44, 1131-1138). Poly(ADP-ribosyl)ation represents a post-translational modification of nuclear proteins involved in DNA repair, DNA replication, and modulation of gene expression. The present study investigates the induction of DNA double-strand breaks and poly(ADP-ribosyl)ation in the renal cortex after in vivo administration of several renal carcinogens to male Wistar rats, and the temporal relationship between these two processes. Dichlorovinylcysteine caused a time-dependent increase in the amount of poly(ADP-ribosyl)conjugates in the kidney cortex, which was preceded by increased formation of DNA double-strand breaks. Potassium bromate and ferric nitrilotriacetate, whose nephrocarcinogenicity is thought to result from increased formation of reactive oxygen species, both induced poly(ADP-ribosyl)ation with the concomitant formation of DNA double-strand breaks. Dimethylnitrosamine, an indirect acting methylating agent, and trimethylpentane, a non-genotoxic renal carcinogen, failed to induce poly(ADP-ribosyl)ation or a significant increase in DNA double-strand breaks in the renal cortex. The results indicate that nephrocarcinogens capable of inducing DNA fragmentation also induce post-translational modification of renal proteins via increased poly(ADP-ribosyl)ation.

Further bioactive acetylenic compounds from the Caribbean sponge Cribrochalina vasculum.

In addition to the known 3-hydroxydocosa-(4E, 15E)-dien-1-yne [1], 3-hydroxy-16-methyleicos-(4E)-en-1-yne [2], and 3-hydroxy-19-methyleicos-(4E)-en-1-yne [3], the lipophilic extract of the Caribbean sponge Cribrochalina vasculum was shown to contain four new bioactive acetylene metabolites, (3R)-hydroxy-14-methyldocos-(4E)-en-1-yne [4], (3R)-hydroxy-16-methyleicos-1-yne [7], (3R)-hydroxy-19-methyleicos-1-yne [8], and docosa-(3E, 15Z)-dien-1-yne [9], whose structures were elucidated on the basis of chemical and spectral studies. The previously unassigned chirality at C-3 of the known compounds 1-3 has been also established as R.

[The mechanism of anticholinesterase action of acetylene organophosphorus inhibitors]. / O mekhanizme antikholinésteraznogo deistviia atsetilenovykh fosforororganicheskikh ingibitorov.

Introduction of the triple bond in the leaving group of the organophosphorus inhibitor molecule gives a sharp raise of the inhibitor activity but does not change principal characteristics of the cholinesterase inhibition mechanism. The reactivation experiments suggest that inactivation of cholinesterases by these compounds occurs due to phosphorylating of the serine hydroxyl by the corresponding phosphoric acid. A close similarity was shown between acetylenic and saturated organophosphorus inhibitors in altering ka upon change of pH and tetraalkylammonium ions action. It is demonstrated that S-alkynyl esters of thioacetic acid are slowly hydrolyzed by acetylcholinesterase and cholinesterase without irreversible inhibition of the enzymes.