Anti-GST Tag polyclonal antibody [HRP]

Phytochemicals are toxic to insects, but their insecticidal efficiencies are usually low compared to synthetic insecticides. Understanding the mechanism of insect adaptation to phytochemicals will provide guidance for increasing their efficacy. Reduced glutathione (GSH) is a scavenger of reactive oxygen species (ROS) induced by phytochemicals. However, in insects, the pathway of GSH biosynthesis in response to phytochemicals is unclear. We found that exposure to 0.5% indole-3-methanol (I3C), xanthotoxin, and rotenone (ROT) significantly retarded the growth of Spodoptera linfra larvae. The oxidative stress in S. linfra larvae exposed to phytochemicals was increased. The up-regulation of glutamate cysteine ligase but not glutathione reductase revealed that the de novo synthesis pathway is responsible for GSH synthesis in phytochemical-treated larvae. Treatment with the inhibitor (BSO) of gamma-glutamylcysteine synthetase (gcic), a subunit of glutamate cysteine ligase, resulted in decreases of GSH levels and GST activities, increases of ROS levels in I3C-treated larvae, which finally caused midgut necrosis and larval death. Treatment with BSO or I3C alone did not cause larval death. The addition of GSH could partly reduce the influence of I3C and BSO on S. linfra growth. Nilaparvata lugens gcic RNAi confirmed the result of BSO treatment in S. litura. N. lugens gcic RNAi significantly increased the mortality of ROT-sprayed N. lugens, in which ROS levels were significantly increased. All data indicate that gcic is involved in insect response to phytochemical treatment. Treatment with dsgcic will increase the insecticidal efficacy of plant-derived compounds.

Aflatoxin B-1 (AFB(1)) is a mycotoxin that is commonly detected in aquatic feed in tropical and subtropical regions. The toxic effects in shrimp and fish tissues following exposure to chronic AFB(1) exposure has been studied but there is no information on tolerance between different species. This study was designed to compare the tolerance of AFB(1) between invertebrate Litopenaeus vannamei and vertebrate Oreochromis niloticus. The emphasis was on growth profile, biotransformation, histopathology and AFB(1) accumulation following exposure to increasing doses of AFB(1). 182 shrimps and 146 tilapia were used and divided into control and AFB(1) exposure groups. Shrimp were exposed to 1.5-fold increasing doses of 1.2, 1.8, 2.7, 4, 6 mg/kg AFB(1) and tilapia to 3.2, 4.8, 7.2, 10.8, 16.2 mg/kg of AFB(1) for 20 d with a 4-day exposure to each AFB(1) with the shrimp/fish sacrificed on the last day of exposed dose(s). At each time point the controls were also sacrificed. A significant decrease in survival rate and weight gain (WG) was observed in shrimp. Higher AFB(1) doses caused a decline in tilapia WG. Dose responsive AFB(1) accumulation was evident in muscle and shrimp hepatopancreas /tilapia liver. The concentration of AFB(1) was significantly higher in shrimp hepatopancreas (22.76-72.89 ng/g) than in tilapia liver (6.68-19.45 ng/g) in spite of exposure to a higher dose regime. The muscle AFB(1) concentration in both species ranged from 0 to 20 ng/g. The shrimp hepatopancreas cytochrome b5 (Cyt b5) concentration increased initially but declined after> 4 mg/kg AFB(1) exposure. The tilapia liver Cyt b5 content declined after> 10.8 mg/kg AFB(1). In the shrimp hepatopancreas, a marked induction of enzymes, aniline hydroxylase (AH), NADPH-cytochrome P450 reductase (NCCR), 7-ethoxyresorufin O-deethylase (EROD), glutathione-S-transferase (GST), sulfotransferase (SULT) and uridinediphosphate glucuronyltransferase (UGT) were observed. Only some of these enzymes, namely, EROD, GST, UGT and SULT but not AH or NCCR were induced in tilapia liver. Hepatopancreas/liver damage in shrimp/fish was marked at higher AFB(1) doses. Marked changes in the shrimp hepatopancreatic cell structure was observed in shrimp at concentrations> 6 mg/kg AFB(1). This study showed that shrimp are more susceptible to AFB(1) than tilapia and further studies are required to determine the role of AH and NCCR enzymes in species differences to AFB(1) toxicity.