heavy metal toxicity due to occupational and domestic exposures raises apprehension over their potential effects on human health and the environment . chronic arsenic toxicity , also known as arsenicosis , is a global health problem affecting millions of people and mainly caused by drinking of arsenic - contaminated ground water . the worst affected countries include india , bangladesh , pakistan , japan , and the united states . arsenic is a naturally occurring metalloid having four primary oxidative states : + 5 , + 3 , 0 , and -3 , among which the trivalent arsenite form ( as2o3 ; as iii ) and the pentavalent arsenate form ( as2o5 ; as v ) are of utmost biological relevance . the inorganic trivalent species of arsenic are of great concern to the toxicologists compared to the organic one . arsenic exposure shows various systemic manifestations , such as pigmentation and keratosis of skin , bronchitis , obstructive and/or restrictive pulmonary diseases , liver disorders allied with non - cirrhotic portal fibrosis , gastrointestinal disorder , polyneuropathy , cancer of various organs like skin , lung , liver , kidney and urinary bladder , anemia etc . arsenic toxicity - acute , subchronic or chronic is known to interfere with hematopoietic and immune systems . the first tissue that encounters arsenic in the body after its systemic absorption is blood . arsenic exposure may lead to its accumulation in erythrocytes and cause anemia associated with leucopenia with characteristic neutrophil depletion and thrombocytopenia . arsenic exerts its toxicity by inactivating numerous enzymes , including the enzymes involved in cellular energy pathways , dna replication , and repair . apart from this , arsenic attacks cellular redox systems resulting in the generation of excess reactive oxygen species ( ros ) in the form of superoxide anion ( o2- ) and hydroxyl radical ( oh ) leading to substantial oxidative damages of proteins , lipids , and dna . as erythrocytes lack any replenishing machinery and have a considerably higher average life of about 120 days , it therefore can carry the impression of long - term toxic and/or pathological insult . moreover , in vitro sodium arsenite even at a very low concentration is reported to induce apoptosis in rat bone marrow mesenchymal stem cells . however , a detailed haematological picture in chronic arsenic intoxication has hardly been reported in toxicological studies . alfa lipoic acid ( ala ) , is an endogenously produced coenzyme and is being used by researchers as a dietary supplement with good bioavailability , both in humans and experimental animals . the role of ala as anti - oxidant and in the prevention of hematological abnormalities caused due to heavy metal toxicity ( such as lead , cadmium and copper ) has been reported earlier and it has been found that the co - administration of ala with heavy metals maintains normal antioxidant activity and normalize hematological parameters , especially anemia , in rats . ala is also reported to prevent arsenic toxicity via protecting against oxidative damages in acute and chronic animal model as well as in vitro studies . a few studies have been undertaken to find the corrective approach of ala on hematological alterations by heavy metals , but protective nature of ala on blood or its components due to subchronic exposure of arsenic in rats are currently lacking . therefore , the aim of the present study is to find out the protective role(s ) of ala , if any , on arsenic - induced hematological alterations and oxidative stress using rats as experimental animal . subchronic arsenicosis was developed in wister rats according to standardized protocol of our laboratory . in short , a dose of as2o3 ( 3 mg / kg body weight / rat / day ) was selected and administered per orally over a period of 28 days . ala was dissolved in olive oil and was administered per orally once daily ( 25 mg / kg body weight / rat ) after about 2 hours of the meal . the dose of ala is calculated keeping the dose for human ( per kg body weight ) essentially as described previously . twenty - four adult male wister rats weighing 13010 g were selected for this experiment . the animals were maintained under standard laboratory conditions ( 14 h light : 10 h dark , 252c ) with free access to food and water . all animal experiments were performed according to the ethical guidelines suggested by the institutional animal ethics committee ( number : 796/ac/03/cpcsea/18 - 01 dated 18.01.2013 ) . rats were randomly grouped into three , consisting eight rats in each group as control ( group i ) , arsenic - treated ( group ii ) , and arsenic - treated and supplemented with ala ( group iii ) . all the animals of groups i , ii and iii were provided with a normal diet composed of 71% carbohydrate , 18% protein , 7% fat , and 4% salt mixture and vitamins . both the group ii and iii rats were gavaged arsenic trioxide solution where only the rats of group iii were given ala per orally after the meal . to overcome the impact of any altered food intake , group i rats were pair - fed with other experimental groups ii and iii . food and water intake and body weight of the rats were monitored throughout the experimental period . blood was collected under sterile condition from anesthetized rats by cardiac puncture and kept in both ethylenediaminetetraacetic acid ( edta ) and heparinized vials for hematological and biochemical analyses , respectively . some portion of edta - treated blood was also used for scanning electron microscopy ( sem ) of erythrocytes . complete blood counts ( total and differential ) and estimation of hematological indices , including total haemoglobin ( hb ) , packed cell volume ( pcv ) , mean corpuscular haemoglobin ( mch ) , mean corpuscular volume ( mcv ) , mean corpuscular haemoglobin concentration ( mchc ) were performed using an automated cell counter ( beckman counter , france ) . neutrophil to lymphocyte ratio ( nlr ) and platelet to lymphocyte ratio ( plr ) were calculated with the help of absolute count of neutrophil , lymphocyte , and platelet . plasma concentration of tas was estimated based on the inhibition of radical cation abts [ 2,2-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid ) radical cation ] , which has characteristic long wavelength absorbance maxima at 734 nm and calculated from trolox standard curve as described earlier . the absorbance of the stock solution containing 7 mm abts ( produced from 12 - 16 hour incubation of 7 mm abts and 2.45 mm potassium persulphate in 0.01 m phosphate buffer saline , ph-7.4 ) was adjusted to about 0.700 at 734 nm with 0.01 m phosphate buffer saline , ph-7.4 . change in absorbance ( a ) was calculated from absorbance reading just before adding sample and after 6 minutes of sample addition was recorded and converted to mm trolox equivalent . tos was estimated according to the method of erel , which is based on the generation of colored complex of ferric ion in the presence of oxidative components and xylenol orange in acidic medium and calculated from h2o2 standard curve . in short , 140 l of sample was added to 900 l of reagent 1 ( containing 150 m xylenol orange , 140 mm nacl and 1.35 m glycerol in 25 mm h2so4 solution , ph 1.75 ) and mixed . the initial reading ( a1 ) was obtained from subtracting absorbance at 800 nm ( secondary wavelength ) from that of 560 nm ( primary wavelength ) . 44 l of reagent 2 ( containing 5 mm ferrous ion and 10 mm o - dianisidine in 25 mm h2so4 solution ) was then added to the above mixture and incubated for 4 minutes . the value of tos was then obtained using a ( = a2-a1 ) from the h2o2 standard curve . oxidative stress index ( osi ) was calculated from the ratio of tos and tas { osi=[(tos , m h2o2 equivalent)100/(tas , m trolox equivalent ) ] } according to the standard method and expressed as arbitrary units . for this purpose , the result unit of tas peripheral blood smear was prepared on grease free glass slides and photographed using zeiss light microscope ( zeiss , thornwood , ny ) and progress capture pro 2.5 software ( genotypic optical systems , gmbh , jena , germany ) using 1000 magnification after staining with the leishmann stain . briefly , erythrocytes were directly fixed overnight with 2.5% glutaraldehyde solution in pbs , ph 7.2 , and post - fixed by keeping overnight in 1% osmium tetraoxide in the same buffer . the suspensions were dehydrated in an ethanol series . after drying with carbon dioxide by the critical point method and sputter coating with gold , samples were examined on a sem ( vegaii lsu , tescan , czech republic ) . one - way anova followed by tukey s hsd post hoc analysis was performed to check any statistical difference between the parameters of the studied groups . statistical analysis was carried out using the statistical program packages spss version 16.0 for windows ( spss inc . , subchronic arsenicosis was developed in wister rats according to standardized protocol of our laboratory . in short , a dose of as2o3 ( 3 mg / kg body weight / rat / day ) was selected and administered per orally over a period of 28 days . ala was dissolved in olive oil and was administered per orally once daily ( 25 mg / kg body weight / rat ) after about 2 hours of the meal . the dose of ala is calculated keeping the dose for human ( per kg body weight ) essentially as described previously . twenty - four adult male wister rats weighing 13010 g were selected for this experiment . the animals were maintained under standard laboratory conditions ( 14 h light : 10 h dark , 252c ) with free access to food and water . all animal experiments were performed according to the ethical guidelines suggested by the institutional animal ethics committee ( number : 796/ac/03/cpcsea/18 - 01 dated 18.01.2013 ) . rats were randomly grouped into three , consisting eight rats in each group as control ( group i ) , arsenic - treated ( group ii ) , and arsenic - treated and supplemented with ala ( group iii ) . all the animals of groups i , ii and iii were provided with a normal diet composed of 71% carbohydrate , 18% protein , 7% fat , and 4% salt mixture and vitamins . both the group ii and iii rats were gavaged arsenic trioxide solution where only the rats of group iii were given ala per orally after the meal . to overcome the impact of any altered food intake , group i rats were pair - fed with other experimental groups ii and iii . food and water intake and body weight of the rats were monitored throughout the experimental period . blood was collected under sterile condition from anesthetized rats by cardiac puncture and kept in both ethylenediaminetetraacetic acid ( edta ) and heparinized vials for hematological and biochemical analyses , respectively . some portion of edta - treated blood was also used for scanning electron microscopy ( sem ) of erythrocytes . complete blood counts ( total and differential ) and estimation of hematological indices , including total haemoglobin ( hb ) , packed cell volume ( pcv ) , mean corpuscular haemoglobin ( mch ) , mean corpuscular volume ( mcv ) , mean corpuscular haemoglobin concentration ( mchc ) were performed using an automated cell counter ( beckman counter , france ) . neutrophil to lymphocyte ratio ( nlr ) and platelet to lymphocyte ratio ( plr ) were calculated with the help of absolute count of neutrophil , lymphocyte , and platelet . plasma concentration of tas was estimated based on the inhibition of radical cation abts [ 2,2-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid ) radical cation ] , which has characteristic long wavelength absorbance maxima at 734 nm and calculated from trolox standard curve as described earlier . the absorbance of the stock solution containing 7 mm abts ( produced from 12 - 16 hour incubation of 7 mm abts and 2.45 mm potassium persulphate in 0.01 m phosphate buffer saline , ph-7.4 ) was adjusted to about 0.700 at 734 nm with 0.01 m phosphate buffer saline , ph-7.4 . change in absorbance ( a ) was calculated from absorbance reading just before adding sample and after 6 minutes of sample addition was recorded and converted to mm trolox equivalent . tos was estimated according to the method of erel , which is based on the generation of colored complex of ferric ion in the presence of oxidative components and xylenol orange in acidic medium and calculated from h2o2 standard curve . in short , 140 l of sample was added to 900 l of reagent 1 ( containing 150 m xylenol orange , 140 mm nacl and 1.35 m glycerol in 25 mm h2so4 solution , ph 1.75 ) and mixed . the initial reading ( a1 ) was obtained from subtracting absorbance at 800 nm ( secondary wavelength ) from that of 560 nm ( primary wavelength ) . 44 l of reagent 2 ( containing 5 mm ferrous ion and 10 mm o - dianisidine in 25 mm h2so4 solution ) was then added to the above mixture and incubated for 4 minutes . the value of tos was then obtained using a ( = a2-a1 ) from the h2o2 standard curve . oxidative stress index ( osi ) was calculated from the ratio of tos and tas { osi=[(tos , m h2o2 equivalent)100/(tas , m trolox equivalent ) ] } according to the standard method and expressed as arbitrary units . for this purpose , the result unit of tas peripheral blood smear was prepared on grease free glass slides and photographed using zeiss light microscope ( zeiss , thornwood , ny ) and progress capture pro 2.5 software ( genotypic optical systems , gmbh , jena , germany ) using 1000 magnification after staining with the leishmann stain . briefly , erythrocytes were directly fixed overnight with 2.5% glutaraldehyde solution in pbs , ph 7.2 , and post - fixed by keeping overnight in 1% osmium tetraoxide in the same buffer . the suspensions were dehydrated in an ethanol series . after drying with carbon dioxide by the critical point method and sputter coating with gold , samples were examined on a sem ( vegaii lsu , tescan , czech republic ) . one - way anova followed by tukey s hsd post hoc analysis was performed to check any statistical difference between the parameters of the studied groups . statistical analysis was carried out using the statistical program packages spss version 16.0 for windows ( spss inc . , assessment of hematological profile indicated that hemolytic and inflammatory responses are the primary events associated with arsenic toxicity in rats after arsenic treatment ( table 1 ) . a significant reduction of erythrocyte count ( p=0.021 ) associated with decreased total hb content ( p=0.031 ) was noticed in arsenic - treated rats compared to that of control . mcv was found to be significantly increased ( p=0.041 ) in arsenic - treated rats compared to that of control , suggesting macrocytosis . in addition , the toxic effect of arsenic also caused significant neutropenia ( p=0.022 ) , lymphocytopenia ( p<0.001 ) , and thrombocytopenia ( p=0.023 ) indicating compromised hemostatic and immune system . eosinophil count shows insignificant increase ( p=0.123 ) whereas monocyte ( p=0.993 ) and basophils ( p=0.684 ) shows insignificant variations after arsenic treatment . neutrophil to lymphocyte ratio ( nlr ) and platelet to lymphocyte ratio ( plr ) , the derived hematological indices representing inflammation , were also altered after arsenic treatment . though nlr showed insignificant elevation ( p=0.330 ) , plr was found to be significantly increased ( p=0.005 ) in arsenic - treated rats . ala supplementation resulted in partial restoration of erythrocyte ( p=0.503 ) , hb ( p=0.180 ) , and mcv ( p=0.807 ) , though insignificant , but leads to significant restoration of lymphocyte count ( p=0.006 ) and thereby partial restoration of total leucocyte count ( p=0.093 ) compared to the arsenic - treated group , but failed to achieve normal status . neutrophil ( p=0.748 ) , eosinophil ( p=0.086 ) , basophil ( p=0.986 ) and monocyte ( p=0.999 ) count does not show any significant improvement . it also significantly reduces the nlr value ( p=0.029 ) associated with a non - significant reduction of plr ( p=0.195 ) compared to the arsenic - treated group . effect of ala supplementation on hematological profile of as2o3 treated male rats data represented as meanstandard error of mean . tukey hsd post hoc analysis , p<0.05 ; control versus treated ; control versus supplemented ; treated versus supplemented hematological alterations were found to be accompanied by poikilocytosis , i.e. morphological alteration of erythrocytes , characterized by the formation of echinocytes and spherocytes and such changes were not seen in the control group ( figure 1a and b ) . the peripheral smear of arsenic - treated rats contains about 19.77% echinocytes and 6.78% spherocytes compared to 1.98% echinocytes and 0.99% spherocytes in control . this morphological response was found to be partially prevented by ala supplementation ( figure 1c ) . ala co - administration reduces the echinocytic content to about 4.69% and that of spherocytes to 1.56% . light microscopic images ( 100 ) of erythrocytes obtained from control ( a ) , arsenic - treated ( b ) , and ala - supplemented ( c ) rats . arsenic - induced echinocytic transformation of erythrocyte was confirmed by sem analysis , which showed distinct membrane blebbing , increased number of spherocytes and microcytosis , but these were almost absent in the control group ( figure 2a and b ) . interestingly , ala supplementation gave substantial protection from arsenic - induced echinocytic transformation ( figure 2c ) . sem images of erythrocytes obtained from control ( a ) , arsenic - treated ( b ) , and ala - supplemented ( c ) rats . echinocytic and microcytic spherocyte transformations of erythrocytes are shown by thick and thin white arrow , respectively . arsenic treatment caused a significant oxidative stress in rats as evident from the elevated plasma tos ( p<0.001 ) , osi ( p<0.001 ) and reduced plasma antioxidant status ( p<0.001 ) compared to the control group . ala , known for its antioxidant potential , was seen to significantly prevent oxidative stress by lowering plasma tos ( p<0.001 ) and osi ( p<0.001 ) status in spite of arsenic supplementation . ala also helped in restoring the antioxidant capacity as shown by a significant increase in plasma tas ( p=0.005 ) in la supplemented group compared to the arsenic group ( figure 3 ) . plasma redox status of control ( a ) , arsenic - treated ( b ) , and ala - supplemented ( c ) rats . assessment of hematological profile indicated that hemolytic and inflammatory responses are the primary events associated with arsenic toxicity in rats after arsenic treatment ( table 1 ) . a significant reduction of erythrocyte count ( p=0.021 ) associated with decreased total hb content ( p=0.031 ) was noticed in arsenic - treated rats compared to that of control . mcv was found to be significantly increased ( p=0.041 ) in arsenic - treated rats compared to that of control , suggesting macrocytosis . in addition , the toxic effect of arsenic also caused significant neutropenia ( p=0.022 ) , lymphocytopenia ( p<0.001 ) , and thrombocytopenia ( p=0.023 ) indicating compromised hemostatic and immune system . eosinophil count shows insignificant increase ( p=0.123 ) whereas monocyte ( p=0.993 ) and basophils ( p=0.684 ) shows insignificant variations after arsenic treatment . neutrophil to lymphocyte ratio ( nlr ) and platelet to lymphocyte ratio ( plr ) , the derived hematological indices representing inflammation , were also altered after arsenic treatment . though nlr showed insignificant elevation ( p=0.330 ) , plr was found to be significantly increased ( p=0.005 ) in arsenic - treated rats . ala supplementation resulted in partial restoration of erythrocyte ( p=0.503 ) , hb ( p=0.180 ) , and mcv ( p=0.807 ) , though insignificant , but leads to significant restoration of lymphocyte count ( p=0.006 ) and thereby partial restoration of total leucocyte count ( p=0.093 ) compared to the arsenic - treated group , but failed to achieve normal status . neutrophil ( p=0.748 ) , eosinophil ( p=0.086 ) , basophil ( p=0.986 ) and monocyte ( p=0.999 ) count does not show any significant improvement . it also significantly reduces the nlr value ( p=0.029 ) associated with a non - significant reduction of plr ( p=0.195 ) compared to the arsenic - treated group . effect of ala supplementation on hematological profile of as2o3 treated male rats data represented as meanstandard error of mean . tukey hsd post hoc analysis , p<0.05 ; control versus treated ; control versus supplemented ; treated versus supplemented hematological alterations were found to be accompanied by poikilocytosis , i.e. morphological alteration of erythrocytes , characterized by the formation of echinocytes and spherocytes and such changes were not seen in the control group ( figure 1a and b ) . the peripheral smear of arsenic - treated rats contains about 19.77% echinocytes and 6.78% spherocytes compared to 1.98% echinocytes and 0.99% spherocytes in control . this morphological response was found to be partially prevented by ala supplementation ( figure 1c ) . ala co - administration reduces the echinocytic content to about 4.69% and that of spherocytes to 1.56% . light microscopic images ( 100 ) of erythrocytes obtained from control ( a ) , arsenic - treated ( b ) , and ala - supplemented ( c ) rats . arsenic - induced echinocytic transformation of erythrocyte was confirmed by sem analysis , which showed distinct membrane blebbing , increased number of spherocytes and microcytosis , but these were almost absent in the control group ( figure 2a and b ) . interestingly , ala supplementation gave substantial protection from arsenic - induced echinocytic transformation ( figure 2c ) . sem images of erythrocytes obtained from control ( a ) , arsenic - treated ( b ) , and ala - supplemented ( c ) rats . echinocytic and microcytic spherocyte transformations of erythrocytes are shown by thick and thin white arrow , respectively . arsenic treatment caused a significant oxidative stress in rats as evident from the elevated plasma tos ( p<0.001 ) , osi ( p<0.001 ) and reduced plasma antioxidant status ( p<0.001 ) compared to the control group . ala , known for its antioxidant potential , was seen to significantly prevent oxidative stress by lowering plasma tos ( p<0.001 ) and osi ( p<0.001 ) status in spite of arsenic supplementation . ala also helped in restoring the antioxidant capacity as shown by a significant increase in plasma tas ( p=0.005 ) in la supplemented group compared to the arsenic group ( figure 3 ) . plasma redox status of control ( a ) , arsenic - treated ( b ) , and ala - supplemented ( c ) rats . in the present study , hematological alterations and associated redox imbalance were seen due to arsenic treatment , which were found to be maintained near normal status after ala supplementation ; also in favour of the contemporary report on the protective potential of ala against arsenic toxicity . the counts of erythrocyte , leucocyte , and platelet along with total hemoglobin content , which were depleted due to arsenic insult showed to be prevented on ala supplementation . although no significant prevention was noted in other hematological indices , but an order of control was seen in this regard due to ala supplementation in arsenic - treated rats . this finding is in partial agreement with related recent reports of hematoprotective effect of ala against heavy metal toxicity , but again , it is to be noted that in these studies ala is used in combination with other drugs . the partial restoration of hematological parameters after ala supplementation is in agreement with previous reports , which show that despite its antioxidant potential , ala fails to significantly improve hematological parameter . arsenic - neutrophil interaction and its deleterious effect on the neutrophils , which potentiates its anticancer activity is well documented in the literature . neutropenia is so profound in arsenic - treated rats that even the ala supplementation fails to restore its count even to near normal . nlr and plr are two derived measures obtained from the neutrophil , lymphocyte , and platelet absolute counts are recently reported as the marker of systemic inflammation and related with disease outcome . recent reports also suggest that nlr is elevated in chronic stress in rats and it can serve the purpose of a physiological marker in experimental animals . both nlr and plr were found to be elevated after arsenic exposure indicating systemic inflammation caused by arsenic toxicity . ala administration significantly reduces these two scores in spite of arsenic exposure even below the status in the sham control group . the differential responses of nlr and plr in the case of arsenic treatment and ala supplementation suggests that in the case of prognosis of arsenic toxicity , a combination of these two should be taken into account as also suggested by other authors . the anti - inflammatory activity of ala in this model of arsenicosis also supports the anti - inflammatory potential as reported in both acute and chronic model in rats . arsenic imposes its damaging effects via impairment of enzyme by forming strong complexes with thiols . it also generates ros during its metabolism in cells leading to redox imbalance and enhanced lipid peroxidation . arsenic - induced oxidative stress and toxicity is bring about by generated free radicals and potentiated by arsenic metabolites especially the organic derivatives of arsenic . dimethylarsine ( a trivalent form of arsenic ) can react with molecular oxygen to form a ( ch3)2as . all these free radicals along with others , like oh ultimately damage various cellular macromolecules , including proteins and dna . generation of ros , beyond the body s endogenous antioxidant balance was known to cause redox imbalance favoring an oxidative milieu . noticeable increase in plasma tos associated with a decrease in plasma tas in comparison to that of the control group indicates a state of oxidative stress due to arsenic toxicity , which further supports the notion that redox imbalance is one of the significant events leading to damages due to arsenicosis . these alterations lead to marked elevation of osi , suggesting a fair reduction of the antioxidant system parallel to increased ros production after arsenic exposure . ala , a naturally occurring antioxidant and coenzyme of many enzymes , includes key enzymes of energy metabolism pathway . ala and its derivative dihydrolipoic acid ( dhla ) quench a number of reactive oxygen species in both lipid and aqueous phases , chelate transition metals , prevent membrane lipid peroxidation along with protein damage via interactions with vitamin c and glutathione and thus they are considered as potent antioxidants . ala shows a significant prevention of redox alteration induced by arsenic treatment , as confirmed by the tos , tas , and osi status in the supplemented group and this is in accordance with other previous reports in this field . these findings / observations suggest that the beneficial effect of ala supplementation in preventing the hematological alteration and inflammatory changes in a rat model of arsenicosis may be attributed to its antioxidant potentials as also suggested by others . microscopic study has shown that arsenic exposure leads to poikilocytic response and reduced discocyte content in rats . the observed major shape transformations being echinocytic and spherocytic , which are in agreement with the previous reports on arsenic affected human populations . sem image analyses confirm these findings and also indicate microcytosis in the arsenic - treated groups . these changes in erythrocyte morphology may be attributed to increased oxidative stress and inflammatory status due to arsenic exposure , which is suggestive of eryptotic changes . oxidative stress within erythrocytes that occurs due to arsenic exposure and accumulation is most likely responsible for membrane injury , methemoglobin formation , osmotic fragility , and destruction of cells . ala treatment ameliorates poikilocytic effect of arsenic and increases discocyte content , reduces microcytosis and membrane blebbing in the peripheral blood . this may be explained by the unique ability of the ala which could neutralize free radicals within aqueous and lipid regions of the cell . this uniqueness of the ala , allows it to be transported easily across the cellular membrane and thereafter alleviate the ros induced damages by its antioxidant capacity and/or by the gsh enhancing ability . in the present study , the use of one selected concentration of ala may not reflect the optimum doses in favour of its ameliorating capacity . moreover , the study could not provide any clue related to its action at the molecular level . this study was also unable to highlight the status of arsenic accumulation in plasma and erythrocytes , though a clear indication exists regarding the hemato - protective ability of ala under arsenic insult . based on the experimental data obtained from the rat arsenicosis model , it may be concluded that ala as a food supplementation has a beneficial effect against arsenic toxicity . it brings about this protection by restoring near normal hematological , oxidative , and inflammatory status . further in - depth studies in this direction may help generating knowledge about the defensive role(s ) of ala against arsenic toxicity .