ABSTRACT
OBJECTIVE To investigate the effects of aerobic exercise on enteric nervous injury in rats exposed to malathion.METHODS Adult male Wistar rats were treated with non-load swi mming every other day,three ti mes a week,each one hour,for six weeks.Before exercise,the rats were trea-ted with malathion 100 mg·kg -1·d -1 by oral gavage,six days a week,for six weeks.The activities of seru m acetylcholinesterase(AChE)and butyrocholinesterase(BuChE)were determined.In addition,the s mall intestinal propulsion indexes were measured.Also,the distribution of nerve plexus in ileu m was observed.The i mmunohistoche mical method was used to measure the levels of protein gene-related petide 9.5 (PGP9.5),substance P (SP),and vasoactive intestinal peptide (VIP).RESULTS Co m-pared with normal control,malathion exposure decreased the activities of seru m AChE and BuChE (P<0.01 ),increased the s mall intestinal propulsion indexes (P <0.05).In addition,the levels of PGP9.5 decreased (P<0.05).At the sa me ti me,the levels of SP increased,and the levels of VIP decreased (P<0.05).Aerobic exercise did not change the activites of cholinesterases,but decreased s mall intes-tinal propulsion indexes,increased the levels of PGP9.5,decreased the levels of SP,and increased the levels of VIP.Co mpared with the malathion exposure only,the rats in malathion ad ministration co mbined with aerobic exercise group de monstrated much lower activites of cholinesterase (P <0.01 ),and the s mall intestinal propulsion indexes decreased fro m (89 ±4)% to (79 ±5)%(P <0.01 ).Moreover,the levels of PGP9.5 increased fro m 0.012 ±0.003 to 0.029 ±0.015 (P <0.01 ).At the sa me ti me,the levels of SP decreased fro m0.174 ±0.067 to 0.1 10 ±0.057(P<0.05),and the levels of VIP increased fro m 0.0076 ±0.0029 to 0.01 1 1 ±0.0047 (P <0.05).The levels of above para meters were sa me or close to those of the normal control.CONCLUSION Malathion exposure induced disorders of enteric nervous syste m in rats,and the aerobic exercise abated the toxic response in enteric nervous syste m of malathion exposure rats.However,these effects were not mediated through recovery of cholinesterases inhibition.