Light micrograph of histological changesof liver of male rat pre and postnatal exposed to 250mg/kg B.W. of BPA shows pyknotic nuclei (arrow),Congested central vein(thick arrow). H&E, 400x. 

Contexts in source publication

Context 1

... high dose (250 mg / kg B. W.) in male rats causes clear congestion of central vein ,the hepatocytes were larger and flattened with clear enlarged pyknotic nuclei .In addition, liver appeared irregular irradiation structure and obvious sinusoidal spaces. (fig-4). ...

Context 2

... rats shows normal, there are trabeculay from capsule dividing the gland into lobules containing mucous secretory units (acini) (fig.13).Very little secretion was founded in light micrograph of prostate removed from rat pre and postnatal exposed to BPA50µg /kg B. W. There is also degeneration of epithelial cell and sloughing of some epithelia. (fig. 14) . BPA led to hyperplasia of lining epithelium and papillary projections toward alveolar lumen with no secretion of prostatic fluid ( fig. 15). The microscopic finding of rat's prostate pre and postnatal treated with BPA 250 mg /kg B. W. shows sever hyperplasia found in most of acini ,the mass of hyperplasia closed the lumen of some ...

Context 3

... aromatase gene expression by neonatalexposure to BPA as reported by (27) couldresult in incomplete differentiation of spermatids in seminiferousepithelium and subsequently resulted in defective spermatogenesisand lowered sperm production as reported by (51). Regarding histopathological finding of liver we observed histopathologicalchanges in liver indicating variable damage after BPAadministration as showed in (Figs.2,3 and 4). Microscopic examinationrevealed that liver could be susceptible to low dosesthis result was reported by several authors, (20and 62). ...

Context 4

... shown in table (1), the weight of liver increased significantly(p ≤ 0.05)due to BPA with high dose 250 mg and 50 mg /kg B.W compared with control group and other treated groups. It seems that the liver weight was not affected by low doses of 50 mg and 50µg /kg B.W BPA compared with control. The oral dosage of 250 mg/Kg BW BPA seems to cause significant increase (p ≤ 0.05) in kidney weight of treated male rats compared with control group, while the other two treated groups have non-significant differences in compared with control group. The kidney weights of treated males with different doses of BPA were not significantly different from each other's. Concerning the means of testis weight of mature F1 male offsprings which pre-and postnatally exposed to (250, 50mg and 50µg/Kg B.W/day50) of BPA. There was significant decrease in testis weight of mature F1 male offsprings pre-and postnatally exposed to BPA at all dose levels when compared with the control group without any significant differences among treated groups.A significant increase (p ≤ 0.05) was shown in prostate weight of male ratspre and postnatally exposed to BPA 250, 50mg and 50 µg /kg B.W (0.361, 0.337 and 0.310) respectively compared with control males (0.147). There were no significant differences in prostate weight among male rats exposed to different doses BPA. Table (3) revealed that the sperm concentration in male rats pre-and postnataly treated with BPA250 and50 mg /kg B.W were significantly decreased ( p ≤ 0.05 ) compared with that of control male rats ,while in the lowestdosès group the decrease doesn't reach the significance(p ≥ 0.05 ) in compared with control group ( table 3). Moreover, there were no significant changes (p≥0.05) among all three treated groups were observed. The results in table(3) indicated a significant increase (p≤0.05) in sperm viability percentage of male rats pre and postnataly exposed to BPA 250,50 mg and 50 µg /kg B.W /day compared with control group . No significant differences among treated groups were shown. Regarding the sperm cell abnormalities, the result of the present study showed a significant increase in the percentage of sperm cell abnormalities in mature F1 male offsprings exposed to BPA(250 ,50 mg and 50 µg/Kg BW/day when compared with control group but the increase of dose was had no significant(p≥0.05) effect on sperm cell abnormalities (table3) The liver tissue examination of the control group has shown histological structure of the liver, the hepatic lobules that consisted of hepatocytes arranged in hepatic cords radiating from the central vein to the periphery of the lobule. The cellular cords were separated by sinusoids (Fig 1). (fig-2) .Liver sections in animals exposed to the dose 50 mg/kg B.W. of BPA have shown irregular arrangement of hepatocyte, enlargement of sinusoid spaces and congestion of central vein ( Fig-3). The high dose (250 mg / kg B. W.) in male rats causes clear congestion of central vein ,the hepatocytes were larger and flattened with clear enlarged pyknotic nuclei .In addition, liver appeared irregular irradiation structure and obvious sinusoidal spaces. ...

Context 5

... kidney tissue examination of the control group has shown histological structure revealed glomeruli with thin glomerular basement membrane, cellularity and patent capsular space surrounding proximal and distal convoluted tubules ( fig. 5).Kidney section from F1 male rats exposed 50 µg / kg B.W. showed dilatation of Bowman's space also enlarged cells lining renal tubules, decrease lumen space and degeneration of lining cell of renal tubules ( figure 6) .The previously exposed male and female rats with this 50 mg/kg/BW. result in obvious histological changes include in renal tubules and in glomeruli . The epithelial cells lining renal tubule were degenerated and necrotic in addition to hemorrhage in the interstitial tissue and narrowing of tubular lumen (star shape) .in addition to presence necrosis in the cells lining glomerular capsule, and sloughing of tubular epithelial cells in tubular lumen ( figure 7).Pre and postnatal exposed F1 male and F1 female rats with high dose250 mg/kg/BW. led to more deleterious histological changes in kidney represented in massive hemorrhagic areas also there were infiltration of the inflammatory cells surrounding thickened blood vessels. The microscopic finding of testes of control rat includes the normal structures of seminiferous tubules shows spermatogenic cells and supporting cells. (fig. 9).The microscopic finding of rat , s testes pre and postnatal treated with BPA50 µg /kg B.W. shows disruption of germinal epithelium which is irregularly placed on the basement membrane with few number of spermatogonia ,sloughing in germinal epithelia also accumulation of pinkish edematous fluid between seminiferous tubules ( fig.10).Histology of rat , s testes pre and postnatal exposed to 50 mg /kg B. W. of BPA shows disarrangement and more sever sloughing of the germinal epithelium and destruction the wall of some seminiferous tubules. There is little number of spermatids in the lumen of seminiferous tubules. (fig.11).Microscopic examination of testes of rats treated withBPA250 mg /kg B. W shows atrophy of seminiferous tubules indicated by increased the interstitial space between the seminiferous tubules and destruction of these tubules ,necrosis and sloughing in the some germinal epithelia. No mature spermatozoa were seen in some the lumens of the seminiferous tubule, (fig.12). Microscopic examination of prostate of control rats shows normal, there are trabeculay from capsule dividing the gland into lobules containing mucous secretory units (acini) (fig.13).Very little secretion was founded in light micrograph of prostate removed from rat pre and postnatal exposed to BPA50µg /kg B. W. There is also degeneration of epithelial cell and sloughing of some epithelia. (fig. 14) . BPA led to hyperplasia of lining epithelium and papillary projections toward alveolar lumen with no secretion of prostatic fluid ( fig. 15). The microscopic finding of rat's prostate pre and postnatal treated with BPA 250 mg /kg B. W. shows sever hyperplasia found in most of acini ,the mass of hyperplasia closed the lumen of some alveoli in addition to presence of papillary projections in other alveoli(fig16). shows of degeneration epithelial cell (thin arrows)and sloughing of epithelia (thick arrows) H&E, ...

Context 6

... results are in agreement with (17and 18). The liver is the major organ for the metabolism and detoxification of xenobiotics, including BPA (19). Therefore, the liver could be largely exposed to BPA, and could be susceptible to lower doses, than other organs (20). Liver enlargement is due to hepatocyte proliferation with the increase in cytochrome P-450 but not fat deposition (21), therefore, increase of relative weight of liver in the present study may be partly related to liver enzyme induction by BPA. The increase in kidney weight was in agreement with results of (22 and 23).increase relative weight of kidney might be caused by defects and disorders in the kidney functions due to the long exposure of kidney cells to the toxic metabolites of BPA for 90 days which resulted in kidney dysfunctions and these findings and after BPA intoxication might be lead to reduced ability of the kidney to eliminate the toxic metabolic substances(24) With regard to effect of BPA on relative testis weight, our results agree with that observed by Nakamura et al. (25) in rat; Wang et al. (26) in mice; Akingbemi et al., (27) in rats Chitra et al. (28) in rat and Kawai et al. (29) in mice and Takahashi and Oishi,( 30) in rat and mice, but these results disagree with that obtained by Kato et al. (31) who found that BPA treatment had no effect on reproductive organs weight of male rats. This decrease in testis weight may be attributed to one of or all the four following reasons: first, during the perinatal period the remethylation process in rat testis mainly occurs during GD 11-15, indicating it may also be affected by BPA exposure (32), therefore, the perinatal exposure to BPA has the potential to modify epigenetic marks in various steroid responsive organs including testis. Second, suppression of normal increase in germ and sertoli cells per testis specially before puberty (33) as the sertoli cells never proliferate after puberty (34).Third, this decrease also may be due to decreased steroidogenic enzyme activity (35 and 36) resulting inhibition of spermatogenesis, which is parallel with histopathological findings observed in our study that revealed defective spermatogenesis and testicular degeneration in testis of mature F1 male rat offsprings exposed to all three doses of BPA, Figs (10 ,11 and 12) .Fourth, it is well known that testicular growth is highly promoted by testosterone and inhibited by estrogen as proved by Balthazart and Hendrick (37) and Zeller (38) and this in coordinate with decrease of testosterone levels in the present study (table2). From table (1) , the prostate corrected weights (g/100g B.W.) of male rats treated with BPA were significantly increased . These findings are consistent with studies by (39; 40 and 41 )Maternal exposure toDES , an increase in free serum E2 and BPA all caused a permanent increase in prostatic androgen receptorsin mice in addition to an increase in adult prosate weight, relativeto negative controls(40;41. , and42). The decreased serum testosterone level (table 2) could be primarilypostulated to the decreased expression of the steroidogeneicenzymes and cholesterol carrier protein ''StAR'' involving thetestosterone synthesis as mentioned by Xi et al. (43) andNakamura et al. (25). Also the reduced serum level of LH (table 2) mightdeteriorate testosterone biosynthesis by adversely affecting theexpression of cholesterol carrier protein or steriodogenic enzymesas mentioned by Nakamura et al. (25). Furthermore BPA isreported to act as antiandrogenic agent blocking the action ofdihydrotestosterone (44). Moreover the testicular response to hCG for progesterone andtestosterone release was found to be decreased or suppressed inBPA treated rats. So these finding , taken all together, suggests thatBPA affect testicular function in term of leydig and sertoli cellfunction leading to inhibition of testosterone secretion ''primarygonadal failure'' (45).On contrary the decreased serum testosterone level disagreewith results obtained by Kato et al. (31) in rats and Kawai et al.(29) in mice, they found that there was non-significant change intestosterone level following BPA exposure when compared withcontrol, but Ramos et al. (46) found that prenatal BPA exposure(25 and 250 μg/kg b.wt) resulted in significant increase in serumtestosterone level at PND 15 when compared with control.This variation may be due to differences in animal species,dose of BPA and time of exposure. The decreased serum LH level (table 2) is similar to the resultsobtained by Nakamura et al. (25); Gharravi et al. (47) andAkingbemi et al. (28). This could be explained by ability of BPAto interfere with LH receptor ligand binding resulting in uncouplingLH from LH receptor that potentially contributes to diminished LHstimulation of steroidogenesis as reported by (48),or due to increased prolactin release after BPA exposure asmentioned by (49), where hyperprolactinemia hasbeen shown to cause reproductive dysfunction as confirmed byKoike et al.(50) and Hamada et al.(51), this dysfunction isnot mediated via direct action on testis but due to its effects at thelevel of hypothalamus-pituitary to inhibit LH-RH and LH secretionas confirmed by (50) and.(52).Controversially these results disagreed with results obtained by(50), who found an increase in serum LH level aftersubcutaneous administration of male rat with 0.3 mg BPA /kg b.wt/day for 2 weeks. This variation in LH level may be attributed tovariation in the doses as clarified by (53) and(54)who mentioned that responses of organs weights and serum hormone levels to estrogen vary in proportion tothe doses, where higher doses decrease LH and very small dosesonly decreases testosterone hormone without response to other.FSH level was unaffected by BPA.These findings are consistent with studies by(55)and (56). Regarding the effects of BPA on epididymal spermcharacters, Theseresults agree with that obtained by (57) in mice;(28) in rat; (58) in rat; (33) in rat and (59)in mice and these resultsdisagrees with that obtained by (31); who found thatBPA administration has no effect on semen picture. This may beattributed to depletion of antioxidant defense system and inductionof oxidative stress as well as increased lipid peroxidation in ratspermatozoa by BPA (28). Lipid peroxidation ishigh toxic to spermatozoa and cause irreversible arrest of spermmotility, decrease sperm count and damage sperm integrity andincreased sperm cell abnormalities which confirmed by (60). Suppressed aromatase gene expression by neonatalexposure to BPA as reported by (27) couldresult in incomplete differentiation of spermatids in seminiferousepithelium and subsequently resulted in defective spermatogenesisand lowered sperm production as reported by (51). Regarding histopathological finding of liver we observed histopathologicalchanges in liver indicating variable damage after BPAadministration as showed in (Figs.2,3 and 4). Microscopic examinationrevealed that liver could be susceptible to low dosesthis result was reported by several authors, (20and 62). In presentstudy; it has been observed that BPA showeddegenerative changes in hepatic cells this also wasreported by (63 ...