DNA copy number variation is long associated with highly penetrant genomic disorders, but it was not until recently that the widespread occurrence of copy number variation among phenotypically normal individuals was realized as a considerable source of genetic variation. It is also now appreciated that copy number variants (CNVs) play a role in the onset of complex diseases. Many of the complex diseases in which CNVs are associated are reported to be influenced by yet to be identified environmental factors. It is hypothesized that exposure to environmental chemicals generates CNVs and influences disease onset and pathogenesis. In this study a proof of principle experiment was completed with ethyl methanesulfonate (EMS) and cytosine arabinoside (Ara-C) to investigate the generation of CNVs using array comparative genomic hybridization (CGH) and the zebrafish vertebrate model system. Exposure to both chemicals resulted in CNVs. CNVs were detected in similar genomic regions among multiple exposure concentrations with EMS and five CNVs were common among both chemicals. Furthermore, CNVs were correlated to altered gene expression. This study suggests that chemical exposure generates CNVs with impacts on gene expression warranting further investigation of this phenomenon with environmental chemicals.

Samuel M. Peterson

Jennifer L. Freeman

Chemical Exposure Generates DNA Copy Number Variants and Impacts Gene Expression

Protective role of 2-imino-4-methyl-1, 2-dihydropyrimido [5, 4C] quinoline-5(6H)-one (IMDHPQ) in indium titanium oxide nanoparticles (InTiO NPs) induced hepatotoxicity was analyzed. InTiO NPs were synthesized and given orally to albino rats to assess their hepatotoxicity. NPs mediated oxidative stress and liver tissue pathology were analyzed. Altered antioxidants (GSH, GPx, and catalase) and, biochemical (SGOT, SGPT, ALP, total protein, and total bilirubin) and histopathological changes were observed due to the oxidative stress caused by InTiO NPs. Varying effects of IMDHPQ on each parameter were observed in the present study. The altered parameters of InTiO NPs exposed rats might be due to the oxidative stress caused by NPs and hepatoprotective or ameliorative efficacy of quinoline compound IMDHPQ on signaling and molecular mechanism needs further study.

Dinesh Bheeman

Sinjula Cheerothsahajan

Sathish Sugumaran

Sankaran Mathan

Ramesh Mathan

Sivanesan Dakshanamurthy

Ranjithkumar Rajamani

Chandar Shekar Bellan

Indium Titanium Oxide Nanoparticles Induced Hepatic Damage: Hepatoprotective Role of Novel 2-Imino-4-methyl-1, 2-Dihydropyrimido [5, 4C] Quinoline-5(6H)-one

Awareness among sewage workers to occupational exposure is growing slowly in many developing countries. Lead (Pb) and cadmium (Cd) are present in sewage water and workers are exposed to these metals as a result of unprotected handling. These heavy metals exposures are responsible for DNA damage and lowering blood total iron (Fe) concentration. Zinc (Zn) is an element for promoting metallothionine expression and binds the free Cd. The total suspended solids (TSS), total dissolved solids (TDS), Pb, and Cd were estimated in sewage water. The whole blood Zn and Fe concentration and Pd and Cd were also estimated. Genotoxicity as indicated by DNA damage was studied by comet assay. It was observed that there were significant differences (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.6617603pt" id="M1" height="9.65971pt" version="1.1" viewBox="-0.0498162 -8.99795 53.2534 9.65971" width="53.2534pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><path id="g113-81" d="M600 480C600 590 528 650 384 650H143L137 622C222 614 225 607 210 531L130 127C113 41 106 36 23 28L17 0H294L300 28C204 36 195 42 212 127L243 284L314 263C327 263 339 263 352 264C465 271 600 337 600 480ZM508 481C508 351 402 304 329 304C289 304 265 311 250 317L295 559C302 594 310 606 323 611C335 616 350 619 367 619C455 619 508 573 508 481Z"/></g><g transform="matrix(.0135,0,0,-0.0135,12.15,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g><g transform="matrix(.0135,0,0,-0.0135,23.887,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g><g transform="matrix(.0135,0,0,-0.0135,30.39,0)"><path id="g113-47" d="M113 -12C146 -12 170 11 170 46C170 78 146 103 114 103S58 78 58 46C58 11 82 -12 113 -12Z"/></g><g transform="matrix(.0135,0,0,-0.0135,33.48,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,39.983,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,46.486,0)"><path id="g113-50" d="M384 0V27C293 34 287 42 287 114V635C232 613 172 594 109 583V559L157 557C201 555 205 550 205 499V114C205 42 199 34 109 27V0H384Z"/></g></svg>) of Pb and Cd concentration in blood for the sewage workers when compared with control population. DNA damage was also observed to be significantly (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.6617603pt" id="M2" height="9.65971pt" version="1.1" viewBox="-0.0498162 -8.99795 53.2534 9.65971" width="53.2534pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><use xlink:href="#g113-81"/></g><g transform="matrix(.0135,0,0,-0.0135,12.15,0)"><use xlink:href="#g117-91"/></g><g transform="matrix(.0135,0,0,-0.0135,23.887,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,30.39,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.0135,0,0,-0.0135,33.48,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,39.983,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,46.486,0)"><use xlink:href="#g113-50"/></g></svg>) higher in the exposed groups but their blood Fe concentration was significantly lower, which may be the reason for their tendency for retention of blood Cd and make them more susceptible. This study also indicated that aged workers had higher blood Zn concentrations as compared to the younger (working &#x3c; 20 years) workers. This may indicate a possible adaptive response. The present study proposes that younger (working &#x3c; 20 years) group is more susceptible as compared to aged group (working &#x3e; 20 years).

Rajlaxmi Basu

Soumendra Nath Talapatra

Aniruddha Mukhopadhyay

Moumit Roy Goswami

Siddhartha Sankar Ray

Prantar Chakrabarti

Shidharth Sankar Ram

Mathummal Sudarshan

Anindita Chakraborty

Anjan Dasgupta

Uday Chand Ghosh

Sila Chakrabarti

Genotoxicity Study with Special Reference to Comet Test in the Blood Cells of Workers Exposed to Sewage Water

Tinospora rumphii (T. rumphii) is a folkloric medicinal plant that is widely distributed in Asia and Africa. It has been widely used by locals to treat many diseases including jaundice, which is a manifestation of liver damage. We investigated the action of T. rumphii crude extract together with zinc sulphate, a known tumor modulator, on hepatic injuries induced by intraperitoneal (i.p) injections of quinoline on albino mice. The hepatotoxic effect was assessed by bilirubin concentration in the blood serum, while the genotoxic effect was determined by single-cell gel electrophoresis (SCGE). The mice orally fed with the crude extracts, following quinoline exposure, had reduced serum bilirubin concentration and DNA damage. Mice treated with Zinc sulphate, on the other hand, had remarkably reduced DNA damage on hepatocytes. Our findings showed that hepatoprotective potential of T. rumphii extract is dose-dependent and that utilization of the extract as medicinal remedy must be strictly monitored, while zinc was proven to reverse genotoxic effect of quinoline. This study unraveled the potential of T. rumphii extract and zinc as important hepatoprotective agents for future treatment of hepatic damage caused by chemotherapeutic agents used in cancer treatment.

Roger Salvacion Tan

Lydia M. Bajo

Modulation of Tinospora rumphii and Zinc Salt on DNA Damage in Quinoline-Induced Genotoxicity and Hepatotoxicity in Male Albino Mice

Acute systemic toxicity via ocular exposure route is not a well understood aspect. Any material/drug/chemical that comes in contact with the eye can evade the first pass metabolism and enter the systemic circulation through the conjunctival blood vessels or via the nasolacrimal route. In this study, the effect of ocular irritant chemicals on the systemic toxicity was assessed in rabbit. Eyes of rabbits were exposed to known ocular irritant (cetyl pyridinium chloride, sodium salicylate, imidazole, acetaminophen, and nicotinamide) for 24&#x2009;h and scored. After a period of 72&#x2009;h, blood was collected from the animals for examining the hematological and biochemical parameters. The animals were then sacrificed and the eyes were collected for histopathology and cytokine analysis by ELISA. Splenocyte proliferation was assessed by tritiated thymidine incorporation assay. The liver and brain of the treated animals were retrieved for evaluating oxidative damage. The chemicals showed moderate to severe eye irritation. Inflammation was not evident in the histopathology but proinflammatory markers were significantly high. The splenocyte proliferation capacity was undeterred. And there was minimal oxidative stress in the brain and liver. In conclusion, acute exposure of ocular irritants was incapable of producing a prominent systemic side effect in the current scenario.

Reshma Sebastian Cherian

Mohanan Parayanthala Valappil

Evaluating Systemic Toxicity in Rabbits after Acute Ocular Exposure to Irritant Chemicals

The state of the art for cell-based in vitro investigations of airborne and inhalable material is &#x201C;air-liquid interface&#x201D; (ALI) technology. Cell lines, primary cells, complex 3D models, or precision-cut lung slices (PCLS) are used to represent the lung or skin by way of an in vitro barrier model. These models have been applied in toxicity or pharmacological testing. However, contrasting with a clear demand for alternative methods, there is still no widely accepted procedure for cell-based in vitro testing of inhalable substances. In the light of this, an analysis was undertaken of common drawbacks of current approaches. Hence, the pivotal improvements aimed at were the cellular exposure environment, overall performance and applicability, operability of online investigations during exposure and routine setup. It resulted in an improved device (P.R.I.T. ExpoCube) based on an &#x201C;all-in-one-plate&#x201D; concept including all phases of the experiment (cell culture, exposure, and read-out) and all experimental groups (two test gas groups, controls) in one single commercial multiwell plate. Verification of the concept was demonstrated in a first experimental series using reference substances (formaldehyde, ozone, and clean air). The resulting ALI procedure enables the application of inhalable substances and mixtures under highly effective exposure conditions in routine utilization.

Detlef Ritter

Jan Knebel

Investigations of the Biological Effects of Airborne and Inhalable Substances by Cell-Based In Vitro Methods: Fundamental Improvements to the ALI Concept

A multimodal approach is effective in analyzing biological problems critically and thus also useful in assessing cytotoxicity under chemicals assaults. In this study effects of isooctane, an organic solvent and component of gasoline produced in petroleum industries, have been explored on normal (HaCaT) and cancerous (HeLa) epithelial cells. Besides morphological alterations, impacts on viability, prime molecular expressions, and bioelectrical properties on exposure to different doses of isooctane were noted. Scanning electron microscopy and viability assay demonstrated remarkable structural alterations and cell death, respectively, in HaCaT but not in HeLa. Transcriptomic and immunocytochemical studies on E-cadherin expression also elucidated pronounced toxic effects on HaCaT. Remarkable changes on the bioelectrical properties (e.g., impedance and phase angle) of the HaCaT, in contrast to HeLa, at different temporal points on isooctane exposure also indicated cytotoxic effects in the former. Hence this study illustrated cytotoxicity of isooctane on HaCaT multidimensionally which was evaded by HeLa.

Lopamudra Das

Sanmitra Basu

Sanghamitra Sengupta

Soumen Das

Jyotirmoy Chatterjee

Differential Effect of Isooctane Doses on HaCaT and HeLa: A Multimodal Analysis

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2 stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death in Arabidopsis leaves. High levels of SO2 caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2 caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+ antagonists EGTA and LaCl3 blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2 and <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-5.76pt" id="M1" height="17.8381pt" version="1.1" viewBox="-0.0498162 -12.0781 47.5186 17.8381" width="47.5186pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><path id="g113-92" d="M290 -163V-135C183 -126 181 -122 181 -44V583C181 662 184 666 290 675V703H120V-163H290Z"/></g><g transform="matrix(.0135,0,0,-0.0135,4.674,0)"><path id="g190-68" d="M614 175C564 76 510 21 408 21C256 21 146 149 146 336C146 488 235 629 402 629C510 629 570 586 597 480L626 488C620 541 614 582 606 638C578 643 510 665 429 665C206 665 44 527 44 316C44 157 153 -15 402 -15C474 -15 558 5 586 11C604 45 629 119 643 165L614 175Z"/></g><g transform="matrix(.0135,0,0,-0.0135,13.806,0)"><path id="g190-98" d="M433 39L423 65C413 59 399 54 387 54C370 54 352 69 352 114V299C352 352 342 392 307 422C285 440 255 449 225 449C168 437 102 399 75 379C56 365 44 353 44 339C44 315 69 296 87 296C101 296 111 303 116 319C124 349 133 371 145 385C156 397 171 404 190 404C241 404 275 364 275 291V274C253 256 180 229 120 209C65 190 39 159 39 110C39 47 88 -12 159 -12C189 -12 237 25 277 52C282 35 288 21 301 8C312 -3 333 -12 348 -12L433 39ZM275 84C256 65 221 48 195 48C164 48 124 73 124 124C124 161 146 180 185 198C206 208 254 229 275 240V84Z"/></g><g transform="matrix(.0095,0,0,-0.0095,19.81,-5.984)"><path id="g50-51" d="M414 144C384 79 371 75 317 75H135L276 221C367 316 408 376 408 465C408 570 327 635 237 635C179 635 131 609 100 575L42 494L67 471C94 510 138 565 205 565C277 565 321 517 321 435C321 348 258 270 195 195C146 137 88 81 33 26V0H411C423 44 433 88 446 135L414 144Z"/></g><g transform="matrix(.0095,0,0,-0.0095,24.428,-5.984)"><path id="g54-36" d="M556 236V289H337V504H275V289H56V236H275V-4H337V236H556Z"/></g><g transform="matrix(.0135,0,0,-0.0135,30.76,0)"><path id="g113-94" d="M226 -163V703H56V676C162 667 165 662 165 584V-43C165 -122 162 -126 56 -136V-163H226Z"/></g><g transform="matrix(.0095,0,0,-0.0095,35.452,3.264)"><path id="g190-100" d="M390 111C344 68 312 56 269 56C212 56 118 102 118 241C118 346 175 401 241 401C277 401 312 388 342 360C350 352 355 349 361 349C372 349 394 371 394 392C394 403 391 411 378 422C362 436 329 449 288 449H287C250 449 190 432 138 392C71 341 37 274 37 197C37 90 112 -12 238 -12C297 -12 363 32 407 90L390 111Z"/></g><g transform="matrix(.0095,0,0,-0.0095,39.616,3.264)"><path id="g190-122" d="M478 437H297V411C355 404 361 392 349 355C329 292 285 174 257 106L167 356C153 394 158 404 205 411L204 437H2V411C57 404 66 391 88 336C117 265 162 144 202 30C208 13 209 0 204 -15C199 -28 191 -49 173 -84C149 -128 130 -153 98 -172C81 -184 73 -193 73 -209C73 -233 101 -257 129 -257C143 -257 156 -252 161 -232C175 -179 197 -122 264 38C333 203 364 286 390 339C417 395 425 403 478 411V437Z"/></g><g transform="matrix(.0095,0,0,-0.0095,43.969,3.264)"><path id="g190-117" d="M298 36L289 62C276 55 253 45 228 45C202 45 169 60 169 141V397H276C289 405 292 426 282 437H169V574L155 576L90 509V437H45L17 408L21 397H90V107C90 28 125 -12 188 -12C198 -12 213 -8 230 1L298 36Z"/></g></svg> elevation. However, EGTA and LaCl3 inhibited SO2-induced <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-5.76pt" id="M2" height="17.8381pt" version="1.1" viewBox="-0.0498162 -12.0781 47.5186 17.8381" width="47.5186pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><use xlink:href="#g113-92"/></g><g transform="matrix(.0135,0,0,-0.0135,4.674,0)"><use xlink:href="#g190-68"/></g><g transform="matrix(.0135,0,0,-0.0135,13.806,0)"><use xlink:href="#g190-98"/></g><g transform="matrix(.0095,0,0,-0.0095,19.81,-5.984)"><use xlink:href="#g50-51"/></g><g transform="matrix(.0095,0,0,-0.0095,24.428,-5.984)"><use xlink:href="#g54-36"/></g><g transform="matrix(.0135,0,0,-0.0135,30.76,0)"><use xlink:href="#g113-94"/></g><g transform="matrix(.0095,0,0,-0.0095,35.452,3.264)"><use xlink:href="#g190-100"/></g><g transform="matrix(.0095,0,0,-0.0095,39.616,3.264)"><use xlink:href="#g190-122"/></g><g transform="matrix(.0095,0,0,-0.0095,43.969,3.264)"><use xlink:href="#g190-117"/></g></svg> increase but did not suppress SO2-induced H2O2 elevation. These results indicate that H2O2 elevation triggered stomatal closure and cell death via <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-5.76pt" id="M3" height="17.8381pt" version="1.1" viewBox="-0.0498162 -12.0781 47.5186 17.8381" width="47.5186pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><use xlink:href="#g113-92"/></g><g transform="matrix(.0135,0,0,-0.0135,4.674,0)"><use xlink:href="#g190-68"/></g><g transform="matrix(.0135,0,0,-0.0135,13.806,0)"><use xlink:href="#g190-98"/></g><g transform="matrix(.0095,0,0,-0.0095,19.81,-5.984)"><use xlink:href="#g50-51"/></g><g transform="matrix(.0095,0,0,-0.0095,24.428,-5.984)"><use xlink:href="#g54-36"/></g><g transform="matrix(.0135,0,0,-0.0135,30.76,0)"><use xlink:href="#g113-94"/></g><g transform="matrix(.0095,0,0,-0.0095,35.452,3.264)"><use xlink:href="#g190-100"/></g><g transform="matrix(.0095,0,0,-0.0095,39.616,3.264)"><use xlink:href="#g190-122"/></g><g transform="matrix(.0095,0,0,-0.0095,43.969,3.264)"><use xlink:href="#g190-117"/></g></svg> signaling in SO2-stimulated Arabidopsis guard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2 production plays critical role in SO2 toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2 production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+ signaling.

Huilan Yi

Xin Liu

Min Yi

Gang Chen

Dual Role of Hydrogen Peroxide in Arabidopsis Guard Cells in Response to Sulfur Dioxide

The investigational anticancer agent batracylin (BAT; 8-aminoisoindolo [1,2-b]quinazolin-10(12H)-one; NSC320846) causes γ-H2AX foci development in exposed tumor cells and has demonstrated activity against solid tumors and adriamycin-resistant leukemia. Reports indicate BAT has wide interspecies variation of adverse effects, including myelosuppression, kidney, bladder, and liver damage, including biliary hyperplasia. The effects of BAT and its metabolite N-acetyl batracylin (NAB) were evaluated in the CFU-GM bone marrow toxicity assay, rat kidney (NRK) cells, bladder epithelial (RBLAK) cells, and rat precision cut liver slices (PCLS). Exposure effects were evaluated biochemically and histologically. Human, dog, and rat exhibited similar CFU-GM IC90 values for BAT (21–29 μM). The ATP assay and γ-H2AX staining showed time- and concentration-dependent toxicity in RBLAK (more severe than NRK at &lt;72 hr) NRK and cells (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.6617594pt" id="M1" height="9.7821pt" version="1.1" viewBox="-0.0498162 -9.12034 55.2661 9.7821" width="55.2661pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><path id="g190-74" d="M303 0V28C221 34 213 39 213 125V525C213 610 221 616 303 622V650H38V622C120 616 128 610 128 525V125C128 40 120 34 38 28V0H303Z"/></g><g transform="matrix(.0135,0,0,-0.0135,4.457,0)"><path id="g190-68" d="M614 175C564 76 510 21 408 21C256 21 146 149 146 336C146 488 235 629 402 629C510 629 570 586 597 480L626 488C620 541 614 582 606 638C578 643 510 665 429 665C206 665 44 527 44 316C44 157 153 -15 402 -15C474 -15 558 5 586 11C604 45 629 119 643 165L614 175Z"/></g><g transform="matrix(.0135,0,0,-0.0135,13.466,0)"><path id="g190-161" d="M130 550H367L393 615L386 623H101L63 323C82 331 123 342 165 342C275 342 328 277 328 188C328 107 283 40 201 40C141 40 99 72 78 91C69 99 59 98 51 91C39 81 30 67 29 58C28 48 33 37 46 24C60 10 104 -12 149 -12C203 -11 269 14 323 59C384 109 412 165 412 225C412 308 347 399 219 399C193 399 146 382 104 367L130 550Z"/></g><g transform="matrix(.0135,0,0,-0.0135,19.78,0)"><path id="g190-254" d="M248 635C97 635 43 457 43 311C43 153 97 -12 247 -12S450 166 450 312C450 466 397 635 248 635ZM246 603C337 603 361 452 361 312S337 20 248 20S132 172 132 313C132 452 156 603 246 603Z"/></g><g transform="matrix(.0135,0,0,-0.0135,30.344,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g><g transform="matrix(.0135,0,0,-0.0135,42.082,0)"><path id="g113-51" d="M412 140C382 77 369 73 315 73H129L270 222C362 320 402 379 402 466C402 571 322 635 234 635C177 635 130 609 99 576L42 495L64 475C90 514 133 568 201 568C274 568 318 519 318 435C318 349 255 267 193 193C144 135 87 78 32 23V0H405C417 45 427 89 440 131L412 140Z"/></g><g transform="matrix(.0135,0,0,-0.0135,48.585,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g></svg> μM after 96 hr BAT exposure). BAT (5 μM and 25 μM) caused biochemical and histology changes to PCLS by day 3 and 25 μM produced centrilobular hepatotoxicity. NAB (≤5 μM) produced no toxicity in CFU-GM, NRK, or RBLAK cells. However, both BAT and NAB caused biliary epithelial cell proliferation in PCLS. Our studies demonstrated species similarities in sensitivity to BAT-induced myelosuppression, and implicate the metabolite NAB in biliary hyperplasia.

Facundo M. Cutuli

Holger P. Behrsing

Compound-Specific Toxicities Detected in CFU-GM, Rat Kidney NRK Cells, Rat Bladder RBLAK Cells, and Rat Liver Slices following Batracylin or N-Acetyl Batracylin Exposure

Paraquat is a bipyridyl herbicide and organic divalent cation which due to its high polarity and water solubility cannot be readily extracted by common organic solvents from body fluids. Dithionite color test for qualitative and quantitative determination of paraquat in urine has been proposed and used for many years. Although some methods were proposed for solvent extraction of paraquat from blood, they are less practical in clinical laboratories and lack high extraction recovery. Clinoptilolite is a highly porous natural zeolite with cation-exchange property and high surface area. In the present work, extraction of paraquat from human blood by clinoptilolite was investigated and compared with Amberlite CG-50 I, a well-known weak cation-exchanger. Blood paraquat was adsorbed by adsorbents (clinoptilolite or Amberlite) and extracted from them by saturated sodium chloride solution. Extracted paraquat was spectrophotometrically measured by means of sodium dithionite reagent at 394.5&#x2009;nm. Recovery, limit of detection, considering signal-to-noise (S/N) ratio of 3, and limit of quantification, regarding S/N of 10, of paraquat extraction by clinoptilolite and Amberlite CG-50 were 81.7&#x25;&#x2009;&#xB1;&#x2009;3.4&#x25;, 0.58&#x2009;&#x3BC;g, and 1.93&#x2009;&#x3BC;g and 83.6&#x25;&#x2009;&#xB1;&#x2009;3.2&#x25;, 0.49&#x2009;&#x3BC;g, and 1.63&#x2009;&#x3BC;g, respectively. Repeatabilities (within-laboratory error) of paraquat extraction by clinoptilolite and Amberlite CG-50 I were 7.1&#x25; and 6.3&#x25;, respectively.

Mohammad-Amin Aghaii-Afshar

Seyed Vahid Shetab-Boushehri

Extraction of Parquat from Blood by Clinoptilolite

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Advances in Toxicology