ABSTRACT
ObjectiveTo observe the morphological feature of myocardial changes in adult rat exposed to citreoviridin(CIT) with selenium and protein deficiency.MethodsAccording to 2 × 2 factorial design,48 healthy male Wistar rats aged 4-week were randomly divided into four groups:group Ⅰ (Se-Pro-CIT+,low selenium and low protein plus CIT group),group Ⅱ (Se-Pro-CIT-,low selenium and low protein without CIT group),group Ⅲ (Se+Pro+CIT+,adequate selenium and adequate protein plus CIT group),and group Ⅳ (Se+Pro+CIT-,adequate selenium and adequate protein without CIT group),12 rats in each group.After one week of normal adaptive feeding,all the rats were fed with selenium and protein deficiency feed for 2 months,and then the animals in group Ⅰ and group Ⅲwere fed with 8 mg·kg-1 ·d-1 of CIT for 2 more months,after that the CIT dose was increased to 10 mg·kg-1 ·d-1 for the final 2 weeks.At the end of the experiment,all the rats were sacrificed by femoral artery bleeding,and body and heart weight were measured.Heart weight index was calculated and histopathological changes were observed under light microscope.Results Heart weight indexes of the 4 groups(Se-Pro-CIT+,Se-Pro-CIT-,Se+Pro+CIT+ and Se+Pro+CIT- groups) were (3.65 ± 0.45) × 10-3,(3.05 ± 0.19) × 10-3,(3.83 ± 1.06) × 10-3 and (3.31 ± 0.52) × 10-3,respectively.The results of factorial analysis showed that the effects of CIT on heart weight index were statistically significant(F =8.524,P ＜ 0.05 ),the effects of Se + Pro were not statistically significant(F =1.347,P ＞ 0.05),and there were no interactions between the two factors (F =0,048,P ＞ 0.05).Morphologically,tissue fibrosis around branch coronary artery in group Ⅰ rats,plenty of cardiocyte pycnosis in group Ⅱ,and myocardial scattered necrotic foci in group Ⅲ were observed,accompanied by inflammatory cell infiltration in group Ⅲ,and normal myocardial structure in group Ⅳ rats.Conclusions Citreoviridin plays a major role in causing myocardial injury( degeneration and necrosis) and CIT combined with selenium and protein deficiency can aggravate the
ABSTRACT
ObjectiveTo clarify the causative effect of citreoviridin toxins(CIT) as well as nutritional deficiency of selenium and protein on rat myocardial injury at biochemical level.Methods According to 2 × 2 factorial design,48 healthy male Wistar rats aged 4-week were randomly divided into four groups:exposed to CIT along with nutritional deficiency of selenium and protein,nutritional deficiency of selenium and protein,exposed to CIT and control groups.After the rats in each group began to be fed with selenium and protein deficiency and(or) adequate fodder for 3 months,8 mg/kg body weight of CIT was fed daily to the rats in the two CIT toxin groups for two months.After that the CIT dose was raised up to 10 mg/kg body weight each day within the final 2 weeks.At the experimental endpoint,all the rats were sacrificed by femoral artery bleeding after ether anesthesia,and serum and heart specimens were collected for biochemical analysis by detecting serum Tn-Ⅰ and albumin,serum activities of CK and GSH-Px,myocardial SOD and T-AOC.ResultsThe interactions between Se & protein and CIT in rat final body weight,serum albumin,and Tn-Ⅰ was observed(F=8.186,6.160,19.183,all P＜ 0.05),whereas interactions in rat body weight of 12 weeks,serum GSH-Px,CK as well as myocardial SOD,T-AOC activity were not found (F=1.633,1.987,0.075,0.474,1.145,all P ＞ 0.05).Under the nutritional deficiency of selenium and protein,serum albumin and Tn-Ⅰ level in the groups with CIT toxin[ (42.88 ± 1.19) g/L,(668.6 ± 55.8) ng/L,respectively]were lower than that of the group without CIT toxin[ (47.59 ± 1.05)g/L,(989.3 ± 49.2)ng/L,respectively,all P ＜0.05].The main effects of selenium and protein on rat body weight of 12 weeks,serum GSH-Px,myocardial SOD and T-AOC were statistically significant between different groups (F =96.860,58.086,4.475,25.485,all P ＜ 0.05).Rat body weights of 12 weeks in the two groups of nutritional deficiency of selenium and protein[ (186.33 ± 7.89),(197.83 ± 7.89)g] were all lower than others[ (274.08 ± 7.89),(265.42 ± 7.89)g,all P ＜ 0.05]; serum GSH-Pxs in the two groups of nutritional deficiency of selenium and protein[ (317.5 ± 102.6),(296.9 ± 90.5)U/L] were all lower than others[ (926.1 ± 110.9),( 1181.7 ± 85.9)U/L,all P ＜ 0.05] ; myocardial SODs in the two groups of nutritional deficiency of selenium and protein [ (65.22 ± 5.91 ) × 106, (62.68 ± 5.61 ) × 106 U/kg] were all lower than others [(74.07 ± 7.24) × 106, (80.07 ± 5.91) × 106 U/kg,all P＜ 0.05]; myocardial T-AOCs in the two groups of nutritional deficiency of selenium and protein[ (1.138 ± 0.086) × 106,(0.806 ± 0.081 ) × 106 U/kg] were all lower than others[(1.688 ± 0.105) × 106,(1.163 ± 0.086) × 106 U/kg,all P ＜ 0.05].Conclusions Animal model with selenium and protein deficiency is successfully established.However,the results of biochemical index tested in the experimental rats show no regularity effect,which needs to be checked again in the future study.