[A new method of bacteriologic control in food preservation industry].
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We investigated the ability of eight food preservatives to induce lipid peroxidation in normal and alpha-linolenic acid (LNA)-loaded cultured rat hepatocytes. On the addition of sodium dehydroacetate (DHA-Na), potassium sorbate (SA-K) or thiabendazole (TBZ) to the cell culture, lipid peroxidation, assessed in terms of the production of malondialdehyde (MDA), was induced in LNA-loaded cells, but not in normal cells. At the low concentrations, induction of lipid peroxidation in LNA-loaded cells was highest with TBZ, whereas at high concentrations DHA-Na greatly induced lipid peroxidation. The occurrence of lipid peroxidation in LNA-loaded cells was accompanied by a decrease in cellular GSH levels with the three preservatives and by a decrease in cellular protein-SH levels with DHA-Na and TBZ. Furthermore, cell injury, measured by the release of LDH, was produced in LNA-loaded cells exposed to DHA-Na and SA-K. The addition of TBZ caused substantial cell injury in normal cells, and even greater injury in LNA-loaded cells. The prevention of lipid peroxidation in LNA-loaded hepatocytes by addition of an antioxidant, N,N'-diphenyl-p-phenylenediamine (DPPD) almost completely prevented DHA-Na- and SA-K-induced cell injury, and reduced TBZ-induced cell injury. The addition of diphenyl (DP), o-phenylphenol (OPP) or butyl p-hydroxybenzoate (BHB) caused severe cell injury, in association with a marked decrease in cellular levels of both of GSH and protein-SH in both groups of cells. However, lipid peroxidation was not detectable in either group of cells exposed to these preservatives. Sodium propionate (PA-Na) and sodium benzoate (BA-Na) had little effect on any cytotoxic parameter in either group of cells.
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In the modern world, as refrigerated storage has replaced lactic acid fermentation methods of food preservation, we no longer ingest large quantities of live lactobacilli with our food, but relatively large numbers of potentially pathogenic Gram-negative bacteria instead. In the brave new world, antibiotics are used as growth-promoting additives in animal feed in every country but Sweden. The antibiotics used in Europe at low dosages, and exempt from prescription requirements, include macrolides, streptogramins and nitro-imidazoles. There is reason to believe that avoparcin, recently banned in Europe as an antibiotic animal feed additive, has contributed to the occurrence of vancomycin-resistant enterococci in humans. Animal foodstuffs production in Europe and the USA is so intensive that it provides very favourable conditions for the spread of bacteria. Pig, cattle and poultry breeding in Europe are beset by formidable difficulties in the form of Salmonella infections, which constitute not only a hygiene but also a clinical problem. Sweden, the bravest of brave new worlds, faces an increase in the influx of domestic animals and foodstuffs from other countries, and in general less restrictive regulations concerning food production and animal husbandry, but reduced powers of control. Thus, we may expect problems both with pathogens (traditional ones such as Salmonella, and potential ones such as food-spoilage Gram-negative bacteria), and with antibiotic-resistant bacteria in our food-stuffs, to become greater.
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Six batches of food traditionally and commonly consumed by southern Chinese, including two samples of dried shrimps and four samples of different species of salted fish, were tested for mutagenic properties using Salmonella typhimurium TA98 and TA1000. Mutagenic activities toward both tester strains were found in all preparations. In most cases, these activities were enhanced by liver microsomal activation. Urine collected from experimental rats regularly fed salted fish also showed mutagenic activity. The level of this activity decreased markedly when the experimental rats were transferred from a salted fish diet to Purina rat chow. Our data suggested the presence of mutagenic/carcinogenic substances in some local preserved foods and at least one of them, salted fish, has been suspected on epidemiological and experimental evidence to be a possible co-carcinogenic factor in the development of nasopharyngeal carcinoma in southern Chinese. Our finding is compatible with this hypothesis.
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The cytogenetic effects of 2(2-furyl)-3-(5-nitro-2-furyl)-acrylamide (AF-2), a food preservative used in Japan, on rat bone marrow cells in vivo were studied. The aberrant metaphase cells in the bone marrow increased and reached the peak level 6 h after intraperitoneal injection of 240 mg/kg body weight of AF-2 and returned to the normal level within 24 h. A dose-response relationship was obtained using 4-240 mg/kg of AF-2. Chromosome aberrations were also induced after oral administration of 30-240 mg/kg. The aberrations were mostly chromatid breaks and the distribution among and within chromosomes was similar to those induced by a carcinogen, 7, 12-dimethylbenz(a)anthracene (DMBA). The present results provide the first evidence of in vivo cytogenetic effects of AF-2 on mammalian cells and, together with the evidence of mutagenicity already proved in other organisms, warn of the possible genetic hazards to cells exposed to this compounds.
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