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Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Unlike earlier hypotheses, there are various methods of testing the effect of free radicals. If the idea is right, then increasing the intake of antioxidants (or other free radical scavangers) ought to increase longevity. In 1968, Harmon found that several antioxidants added to mouse diets, 2-mercaptoethylamine (2ME) and BHT (butylated hydroxytoluene), increased mean survival time by 29% with 2ME.134 No increase in maximum lifespan was noted and four other antioxidants were ineffective. Georgieff noted that free radical inhibitors such as vitamins A and C, and copper also inhibit cancerigenesis.135 Many, not all, of the the in-use anticancer drugs are also free radical inhibitors. Comfort et al. fed ethoxyquin, an antioxidant to mice and got about 100 days’ extension of lifespan (18%).136 As Comfort et al. comment, such studies do not prove (nor disprove) the free radical hypothesis. Perhaps the bad taste means less food consumption, and thus a covertly restricted diet. Or perhaps excess antioxidant destroys toxic elements in the food, or induces an increase in enzyme concentrations, etc.
Chemical Leukoderma (Depigmentation)
Published in Francis N. Marzulli, Howard I. Maibach, Dermatotoxicology Methods: The Laboratory Worker’s Vade Mecum, 2019
Howard I. Maibach, Jorge R. Toro, Gerald A. Gellin, Leslie P. McCarty
No depigmentation was induced when tested with the following substances on black guinea pigs and black mice: B HA, BHT, octyl and propyl gallate, ethoxyquin, gum guaiac, diethylamine hydrochloride, dilaurylthiodiproprionate, nonylphenol, ophenylphenol, p-phenylphenol, octyl phenol, NDGA, and tocopherol.
Inhibition of Colon Carcinogenesis*
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
The phenolic antioxidants, butylated hydroxyanisole (BHA) and butylated hydrox-ytoluene (BHT), as well as the nonphenolic antioxidant, ethoxyquin, all inhibit colon carcinogenesis. In one experiment45 with BHT male F344 rats were injected for 10 weeks with 7.4 mg azoxymethane per kilogram body weight. Provision of 6600 ppm BHT in the diet concurrently with the carcinogen reduced the colon tumor incidence from 87% (AOM controls) to 58%. On the other hand, administration of BHT after AOM treatment did not affect the tumor incidence but did increase the total number of tumors from 28 in AOM controls to 40. The high level of BHT used was mildly toxic as indicated by a lower weight gain of BHT rats compared to controls. In a more recent study46 concurrent administration of 0.75% BHT in the diet while injecting BALB/c mice with 20 mg DMH per kilogram body weight was carried out. The colon tumor incidence was reduced in males (75 to 34%, p = 0.0036), but was not significantly reduced in females (60 to 50%). Hence, a sex-specific protective effect of BHT was observed. In a third study47 concurrent administration of 0.5% BHT to the diet of male Sprague-Dawley rats treated with 20 mg DMH per kilogram for 20 weeks also reduced the colon tumor incidence. There are probably several mechanisms of BHT inhibition that will be elucidated. As a free radical scavenger BHT could remove activated metabolites of DMH, prevent DNA insult, and thus reduce the tumor incidence. Support for this hypothesis comes from reports that BHT decreases the binding of acetylaminofluorene and its metabolites to DNA,48 that BHT reduces carcinogen-induced chromosomal breakage,49 and that BHT reduces the binding level of DMH to DNA in colon expiants.39 Furthermore, BHT enhances glutathione S-transferase activity suggesting its involvement with detoxification reactions of DMH.
Emerging pharmacological strategies for the management of chemotherapy-induced peripheral neurotoxicity (CIPN), based on novel CIPN mechanisms
Published in Expert Review of Neurotherapeutics, 2020
Andreas A. Argyriou, Jordi Bruna, Susanna B. Park, Guido Cavaletti
However, a high throughput drug screen in a DRG neuron line treated with paclitaxel identified ethoxyquin as the most effective neuroprotective compound. Tellingly, ethoxyquin seems to be a chaperone HSP90 inhibitor by reducing the levels of two of its client proteins, i.e. SF3B2 and ataxin-2 [49]. A subsequent study by the same group also confirmed its usefulness by the same mechanism following cisplatin treatment [50]. Significantly, HSF-1 drives a transcriptional program distinct from HSP in normal cells to support cancer cells, and the HSP inhibitors are under investigation as cancer co-treatments [51,52]. Figure 1 schematically depicts the emerging therapeutic targets that are currently being evaluated in the CIPN setting, based on novel mechanisms.
The effects of aflatoxin residues on nutritional contents in ground red chili peppers (Capsicum annuum)
Published in Toxin Reviews, 2020
Ozgur Kuzukiran, Ayhan Filazi, Begum Yurdakok-Dikmen, Gorkem Ozansoy-Cengiz, Ismayil Safa Gurcan, Ercan Karabulut, Ufuk Tansel Sireli
The use of carotenoids in the control of growth of AF-producing fungi is still controversial. Norton (1997) argues that the growth of A. flavus is not affected by carotenoids. Conversely, Capsanthin (Masood et al.1994), and capsantal (a commercial product containing red pepper extract, ethoxyquin and excipient) (Santos et al.2010) were suggested to prevent the growth of A. flavus. However, Santos et al. (2010) showed that although capsantal inhibits the growth of A. flavus, it does not affect AF production and AF production depends on temperature and time. In our study, no such relationship was found between the AFs and the carotenoids (capsaicinoids and total carotenes) in the samples (Table 3). Conversely, the frequency of AF contamination was highest in peppers containing the highest concentration of capsaicin. So, as claimed by Santos et al (2010), the AF accumulation in the samples may have been influenced by external factors (temperature and time) rather than internal factors. Thus, it was concluded that the growth of fungi and AF production can be limited if the peppers are stored at normal industrial storage temperatures (10 °C).