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This article summarized the use of guanidine disinfectants in China and the use of guanidine cationic disinfectants, polyhexamethylene guanidine (PHMG), in South Korea, which had caused severe lung damage events such as pulmonary fibrosis. The authors reviewed the studies that Chinese scientists employed ultrasonic atomization technology to simulate the actual scenario of human exposure to PHMG and proved the findings that PHMG could cause pulmonary fibrosis. These results could highlight the necessity of full attention to lung damage caused by guanidine disinfectants and its mechanism, so as to provide the important scientific basis for the protection of public health safety and the formulation of corresponding policies.
ABSTRACT
This article summarized the use of guanidine disinfectants in China and the use of guanidine cationic disinfectants, polyhexamethylene guanidine (PHMG), in South Korea, which had caused severe lung damage events such as pulmonary fibrosis. The authors reviewed the studies that Chinese scientists employed ultrasonic atomization technology to simulate the actual scenario of human exposure to PHMG and proved the findings that PHMG could cause pulmonary fibrosis. These results could highlight the necessity of full attention to lung damage caused by guanidine disinfectants and its mechanism, so as to provide the important scientific basis for the protection of public health safety and the formulation of corresponding policies.
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Objective To evaluate the effect of aminoguanidine on cell apoptosis induced by acute myocardial ischemia in rats.Methods Thirty adult male Sprague-Dawley rats,weighing 250-290 g,were randomly divided into 3 groups (n =10 each):sham operation group (group S),myocardial ischemia group (group Ⅰ),and aminoguanidine group (group AG).The model of acute myocardial ischemia was established by ligating the left anterior descending branch of the coronary artery of rats anesthetized with chloral hydrate.Aminoguanidine 100 mg/kg was intraperitoneally administrated at 6 h of ischemia in AG group,while the equal volume of normal saline was given instead of aminoguanidine in group Ⅰ.The chest was opened at 3 h after aminoguanidine administration and hearts were quickly removed for detection of apoptosis in cardiomyocytes (by TUNEL) and expression of Bcl-2 and Bax in cardiomyocytes (by immuno-histochemistry),and for microscopic examination with light microscope.Apoptotic rate was calculated.Results Compared with group S,the apoptotic rate was significantly increased,the expression of Bax was up-regulated,and the expression of Bcl-2 was downregulated and the ratio of Bcl-2/Bax was decreased in group Ⅰ.Compared with group Ⅰ,the apoptotic rate was significantly decreased,the expression of Bax was down-regulated,and the expression of Bcl-2 was up-regulated,and the ratio of Bcl-2/Bax was increased in group AG.The pathological changes of myocardial cells were significantly attenuated in AG group as compared with group Ⅰ.Conclusion Amionguanidine can inhibit apoptosis in cardiomyocytes and is helpful in mitigating injury induced by acute myocardial ischemia in rats.
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ObjectiveTo evaluate the effect of aminoguanidine on expression of inducible nitric oxide synthase (iNOS) in neurons in the small intestinal nerve plexus of starved rats.MethodsNinety male SD rats weighing 230-270 g were randomly divided into 3 groups:group normal control (group C,n =10) ; group starvation (group S,n=40) and group starvation + aminoguanidine (group A,n =40).The animals were allowed free access to water but no food during starvation in S and A groups.In group A the animals were given aminoguanidine 150 mg·kg-1 ·d-1 intraperitoneally during starvation.Ten animals were sacrificed at 3,5,7 and 9 d of starvation respectively and intestine specimens were taken for determination of ratio of intestinal transit using dextran blue-2000 as indicator.Then the specimens of intestinal myenteric nerve plexus of ileum were collected and stained by histochemistry with nicotinamide-adenine dinucleotide phosphate-d for determination of iNOS expression.ResultsStarvation significantly reduced the small intestinal transit and increased iNOS expression in neurons in the myenteric nerve plexus of small intestine in proportion to days of starvation in group S compared with group C.Intraperitoneal aminoguanidine significantly attenuated the starvation-induced changes in intestinal transit and iNOS expression.ConclusionAminoguanidine can attenuate the up-regulation of the expression of iNOS in neurons in the myenteric nerve plexus of small intestine induced by starvation and is helpful in promoting the intestinal transit in starved rats.
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Objective:To investigate the expression of receptor for advanced glycation end products (RAGE)in the thyroid tissue of diabetes mellitus (DM)rats.Methods:The rat model of DM was established by high-lipid diet and vena caudalis injection of streptozocin.The rats of DM models were then randomly divided into three groups:DM group(n=17),insulin intervention group(n=16)and aminoguanidine intervention group(n=16).Nine normal rats were taken as controls.Twelve weeks after the establishment of DM model,rats were sacrificed and the thyroid tissue was taken to determine RAGE mRNA and the protein expression with the method of RT-PCR and Western Blot.Results:The levels of RAGE mRNA and protein expression were higher in the thyroid tissue of DM rats than those in controls (P＜0.05).The levels of RAGE mRNA and protein expression were lower in the thyroid tissue of insulin intervention group and aminoguanidine intervention group than thor of DM group (P＜0.05).Conclusion:The levels of RAGE mRNA and protein expression were up-regulated in the thyroid tissue of DM rats,which can be restrained by controlling blood glucose and blocking the formation of advanced glycation end products.
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Objective To investigate the protective effect of aminoguanidine(AG),silymarin (Sil) and anisodamine (Ani) on retinal capillary pericytes cultured in glycosylation products. Methods MTT cololrimetric assay, thymidine incorporating and fluorescent indicator fura 2 acetoxy methyl ester (Fura 2AM) were used to study the influence of AG,Sil and Ani on the growth,DNA synthesis,and cytosolic free calcium([Ca 2+ ]i)changes of pericytes cultured in the medium contained early glycation products (EGs) or advanced glycation end products (AGEs). Results Cultured in the medium contained EGs,the A value by MTT assayed and amount of thymidine incorporating in AG group and Sil group were obviously elevated than those of control group(P
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Objective To evaluate the effect of aminoguanidine (AG) on neuronal apoptosis induced by focal cerebral ischemia in rats and the possible mechanism of protective effect of AG against cerebral ischemic injury.Methods Fifty-four male SD rats weighing 250-290 g were randomly divided into 3 groups: (1) sham operated group (SH group, n = 18); (2) ischemic group (IS group, n = 18) and (3) AG group(n = 18). SH, IS and AG groups were further divided into 3 subgroups according to the administration time:2, 6 or 12 h following cerebral ischemia. In AG group AG 100 mg? kg-1 was given intraperitoneally twice a day for 3 consecutive days. In IS group normal saline was given instead of AG. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO). A nylon thread with rounded tip which was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Homer's syndrome and right side hemiplegia. In SH group the carotid artery was exposed but no thread was inserted. The nylon thread was with drawn to allow reperfusion after 2, 6 or 12 h MCAO. The animals were detected by flow cytometry. Results Significantly increased DNA fragmentation indicative of apoptosis was detected after MCAO. The percentage of apoptotic cells and expression of Bax protein were significantly lower after 2, 6 and 12 h ischemia in AG group than in IS group but still significantly higher than in SH group. The expression of Bcl-2 protein was significantly higher after 2,6 and 12 h in AG group than in IS group. There was no significant difference in the expression of Bcl-2 protein between IS and SH group. Conclusion AG can protect neurons from apoptosis through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.