Toxicological evaluation of Phospholipase D from Kitasatospora paracochleata

Author(s):  
Kevin J. Matten ◽  
Alastair Mak



2020 ◽  
Vol 77 (2) ◽  
pp. 353-360
Author(s):  
Nadia Malik ◽  
Mahmood Ahmad ◽  
Muhammad Minhas ◽  
Ruqia Tulain ◽  
Ikrima Khalid ◽  
...  


2011 ◽  
Vol 4 (5) ◽  
pp. 26-30 ◽  
Author(s):  
Cherif H.S Cherif H.S ◽  
◽  
Saidi F Saidi F ◽  
Guedioura A Guedioura A


2015 ◽  
Vol 43 (1) ◽  
pp. 174-181
Author(s):  
Marwah M ◽  
Hanan Mahmoud ◽  
Mona El-Shehedi ◽  
Namaa Mohamed


2019 ◽  
Vol 14 (7) ◽  
pp. 649-657 ◽  
Author(s):  
Li Li ◽  
Jiemin Li ◽  
Jian Sun ◽  
Ping Yi ◽  
Changbao Li ◽  
...  

Background: Phospholipase D (PLD)is closely related to browning and senescence of postharvest longan fruit. Objective: This study investigated the effects of 2-butanol (a PLD inhibitor) on the expression and regulation of PLD during storage of longan fruit at a low temperature. Methods: Senescence-related quality indices showed that the 2-butanol-treated fruit presented lower pericarp browning index, pulp breakdown index and total soluble solid value than the untreated fruit. Results: The fruit treated by 60 µL/L 2-butanol exhibited the strongest inhibition on senescence, which significantly delayed changes in weight, titratable acidity content, total soluble solid content and ascorbic acid content. This treatment maintained a high level of total phenolic content and caused significant inhibition on pericarp browning and pulp breakdown. Through ELISA method, 60 µL/L 2-butanol treatment also reduced PLD activity. Real-time RT-PCR (RT-qPCR) results showed that PLD mRNA expression level was inhibited by 60 µL/L 2-butanol within 15 days. Western-blotting results further confirmed the differential expression of PLD during storage, and a relatively higher expression for PLD protein was found in control compared to the 2-butanoltreated fruit during 15-d storage. Conclusion: These results provided a scientific basis and reference to further investigating postharvest longan quality maintenance by regulating the PLD gene expression.



2019 ◽  
Vol 19 (5) ◽  
pp. 667-676
Author(s):  
José R. Santin ◽  
Gislaine F. da Silva ◽  
Maria V.D. Pastor ◽  
Milena F. Broering ◽  
Roberta Nunes ◽  
...  

Background: It was recently demonstrated that the phthalimide N-(4-methyl-phenyl)-4- methylphthalimide (MPMPH-1) has important effects against acute and chronic pain in mice, with a mechanism of action correlated to adenylyl cyclase inhibition. Furthermore, it was also demonstrated that phthalimide derivatives presented antiproliferative and anti-tumor effects. Considering the literature data, the present study evaluated the effects of MPMPH-1 on breast cancer bone metastasis and correlated painful symptom, and provided additional toxicological information about the compound and its possible metabolites. Methods: In silico toxicological analysis was supported by in vitro and in vivo experiments to demonstrate the anti-tumor and anti-hypersensitivity effects of the compound. Results: The data obtained with the in silico toxicological analysis demonstrated that MPMPH-1 has mutagenic potential, with a low to moderate level of confidence. The mutagenicity potential was in vivo confirmed by micronucleus assay. MPMPH-1 treatments in the breast cancer bone metastasis model were able to prevent the osteoclastic resorption of bone matrix. Regarding cartilage, degradation was considerably reduced within the zoledronic acid group, while in MPMPH-1, chondrocyte multiplication was observed in random areas, suggesting bone regeneration. Additionally, the repeated treatment of mice with MPMPH-1 (10 mg/kg, i.p.), once a day for up to 36 days, significantly reduces the hypersensitivity in animals with breast cancer bone metastasis. Conclusion: Together, the data herein obtained show that MPMPH-1 is relatively safe, and significantly control the cancer growth, allied to the reduction in bone reabsorption and stimulation of bone and cartilage regeneration. MPMPH-1 effects may be linked, at least in part, to the ability of the compound to interfere with adenylylcyclase pathway activation.



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