Dietary exposure to ochratoxin A reduces growth performance and impairs hepatic purinergic signaling in tambaqui (Colossoma macropomum)

2020 ◽  
Vol 46 (6) ◽  
pp. 2055-2064
Author(s):  
Matheus D. Baldissera ◽  
Carine F. Souza ◽  
Jefferson A. da Silva ◽  
Danilo C. Barroso ◽  
Eduardo M. Glória ◽  
...  
Author(s):  
Iurych Nicolau Barros Bussons ◽  
Elcimar da Silva Souza ◽  
Paulo Henrique Rocha Aride ◽  
Wallice Luiz Paxiúba Duncan ◽  
Jackson Pantoja-Lima ◽  
...  

2016 ◽  
Vol 98 ◽  
pp. 127-133 ◽  
Author(s):  
Bui Thi Mai Huong ◽  
Le Danh Tuyen ◽  
Do Huu Tuan ◽  
Leon Brimer ◽  
Anders Dalsgaard

Toxins ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 795
Author(s):  
Manar Al Ayoubi ◽  
Mohammad Salman ◽  
Lucia Gambacorta ◽  
Nada El Darra ◽  
Michele Solfrizzo

The present study investigated the dietary and urinary OTA occurrence among 44 Lebanese children. Relying on HPLC-FLD analysis, OTA was found in all the urine samples and in 46.5% and 25% of the 24 h duplicate diet and dinner samples, respectively. The means of OTA levels in positive samples were 0.32 ± 0.1 ng/g in 24 h diet, 0.32 ± 0.18 ng/g in dinner and 0.022 ± 0.012 ng/mL in urines. These values corresponded to margin of exposure (MOE) means of 7907 ± 5922 (neoplastic) and 2579 ± 1932 (non-neoplastic) calculated from positive 24 h diet, while 961 ± 599 (neoplastic) and 313 ± 195 (non-neoplastic) calculated from the urine. Since the MOE levels for the neoplastic effect were below the limit (10,000), a major health threat was detected and must be addressed as a health institutions’ priority. Besides, the wide difference between PDIs and MOEs calculated from food and urine suggests conducting further OTA’s toxicokinetics studies before using urine to measure OTA exposure.


2017 ◽  
Vol 106 ◽  
pp. 202-208 ◽  
Author(s):  
Ali Heshmati ◽  
Tahereh Zohrevand ◽  
Amin Mousavi Khaneghah ◽  
Amir Sasan Mozaffari Nejad ◽  
Anderson S. Sant’Ana

Toxins ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 480 ◽  
Author(s):  
Diana Herman ◽  
Peter Mantle

Ochratoxin A is best known as a potent renal carcinogen in male rats and mice after necessarily protracted ingestion, although valid extrapolation to any human disease has not been verified. The hypothesis that the toxin is a cause of human testicular cancer was proposed a decade ago and has proliferated since, partly through incomplete study of the scientific literature. Archived tumorous rat testes were available from Fischer F344 rats exposed to continuous dietary exposure for half of or the whole life in London in the 2000s. Renal cancer occurred in some of these cases and testicular tumours were observed frequently, as expected, in both treated and untreated animals. Application of clinical immunohistochemistry has for the first time consistently diagnosed the testicular hypertrophy in toxin-treated rats as Leydig cell tumours. Comparison is made with similar analysis of tumorous testes from control (untreated) rats from U.S. National Toxicology Program studies, both of ochratoxin A (1989) and the more recent one on Ginkgo biloba. All have been found to have identical pathology as being of sex cord-stromal origin. Such are rare in humans, most being of germinal cell origin. The absence of experimental evidence of any specific rat testicular cellular pathology attributable to long-term dietary ochratoxin A exposure discredits any experimental animal evidence of testicular tumorigenicity. Thus, no epidemiological connection between ochratoxin A and the incidence of human testicular cancer can be justified scientifically.


Food Control ◽  
2020 ◽  
Vol 112 ◽  
pp. 107108 ◽  
Author(s):  
Tuan Huu Do ◽  
Son Cao Tran ◽  
Chi Dinh Le ◽  
Ha-Binh Thi Nguyen ◽  
Phuong-Thao Thi Le ◽  
...  

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