Hydrolytic rancidification:

This is the process by which water is introduced into the oil and causes rancidity. Three water molecules (H₂O) each ‘donate’ one of their 2 hydrogen atoms to the fatty acid structure at the site where the glycerol backbone of the fatty acid is attached to the carboxylic acid. This detaches the backbone and creates free carboxylic acids which have unpleasant taste and smell, and robs many polyunsaturated oils of their health benefits. Compared with oxidative rancidity (see below), this reaction is slower and easier to control, but can be accelerated by the presence of micro-organisms or enzymes.

Oxidative rancidification

Oxidative rancidification is more rapid than hydrolytis rancidification, and in polyunsaturated oils is impossible to control entirely. It occurs when oxygen is introduced into the polyunsaturated fatty acid at a site of a double bond (see Figure 2), creating the ‘hydroperoxide free radical’. This free radical is very destructive and floats through the oil ripping off electrons wherever it finds them, leaving aldehydes, ketones and carboxylic acids in its wake. These compounds give an off-flavour to the oil and, like hydrolysis above, reduces the health benefits of the oil.

Protecting oils against rancidity

The antidote to oxidation are the anti-oxidants. Anti-oxidants, as their name implies, specifically target the free radicals caused by oxidation and reverse much of the damage that they cause. They are able to do this because they also contain unpaired electrons and can either donate electrons to the oxidized fatty acids or extract an unpaired electron to prevent oxidation. In the process, the antioxidant is itself

The Canadian Food Inspection Agency (Feeds Section) allows the inclusion of BHT and BHA in animal feeds without registration, at a maximum inclusion rate of 0.02% of the total fat or oil content of the complete feed.  Both of these phenolic compounds are listed as GRAS (Generally Recognized as Safe) and are ubiquitously found in horse feeds and supplements.  There is a vigorous, perennial debate about the safety of these synthetic antioxidants. The first technical report of possible carcinogenicity related to these compounds appeared in 1983.  Ito et al. (1983) found that BHA caused cancer in the forestomach of rats at a dietary inclusion rate of 2%.  Three years later, BHT was found to be associated with stomach cancer in rats at dietary inclusion rate of 0.5% (Olsen et al., 1986).  These studies launched a major effort on the part of the Canadian Health Protection Branch (HPB) to evaluate the potential risk of BHA and BHT to humans.  These studies all were conducted over a period of 9 to 27 days, and the maximum safe dose of BHA was determined to be 0.25% inclusion rate (Umemura et al., 2001).  The HPB maintained that both these compounds were safe for human consumption, because the cancerous lesions appeared to be species-specific (ie. only toxic to mice).  Research has also demonstrated that BHT is associated with alveolar tumors too (Witschi 1986), apparently by instigating an inflammatory response in the lung (Kupfer et al., 2002; Sun et al., 2003; Bauer et al., 2001).  In addition, the lung toxicity demonstrated with BHT appears to be enhanced by simultaneous exposure to BHA (Yamamoto et al., 1988).  However, reviews of the literature have concluded that the toxicity of BHA and BHT is species-specific, and not relevant to humans (Whysner and Williams 1996).  But is it relevant to horses? The horse is a hind-gut fermenter, and is therefore anatomically and functionally distinct from humans – and from most rodents.  If we can discount the toxicity of BHA and BHT to humans as irrelevant based on species-specificity, we must, by the same argument, be wary of potential toxicity in other species such as the horse.  In the absence of species-specific toxicology data, the best advice is to make yourself aware of the possible toxic consequences of these preservatives.  Find out if your horse feed and/or supplements contain BHT or BHA, and make pragmatic efforts to reduce total exposure to a minimum.

Natural, fat-soluble antioxidants are available and may be an effective strategy for preserving oils. In some cases, vitamin A (beta carotene) or vitamin E (alpha tocopherol) may be useful for stabilizing polyunsaturated oils. Phenolics from plants are a very interesting source for antioxidants, including rosmarinic acid and lipophilic flavonoids (Mimica-Dukic and Bozin 2008). There is no information in the scientific literature pertaining to how well these compounds are able to preserve polyunsaturated oils.

Owing to the inherent instability of polyunsaturated oils and their inclination to oxidation, many dietary polyunsaturated oils are fortified with some sort of antioxidants. However, this is not a particularly good way to deliver antioxidants to the horse; the reason for this is that antioxidants are themselves oxidized in the presence of free radicals and there is high turnover of oxidation status of antioxidants in such a matrix. There would be greater benefit to delivering stabilized antioxidants directly to the horse, rather than providing them in oil.

References

Bauer AK, Dwyer-Nield LD, Keil K, Koski K, Malkinson AM. (2001) Butylated hydroxytoluene (BHT) induction of pulmonary inflammation: a role in tumor promotion. Exp Lung Res;27(3):197-216.

Ito, N., Fukushima, S., Hagiwara, A., Shibata, M., Ogiso, T.  (1983)  Carcinogenicity of butylated hydroxyanisole in F344 rats.  J Natl Cancer Inst, 70:343-352.

Iverson, F.  (1995)  Phenolic antioxidants: health protection branch studies on butylated hydroxyanisole.  Cancer Let, 93:49-54.

Kupfer, R., Dwyer-Nield, L.D., Malkinson, A.M., Thompson, J.A.  (2002)  Lung toxicity and tumor promotion by hydroxylated derivatives of 2,6-di-tert-butyl-4-mehtylphenol (BHT) and 2-tert-butyl-4-methyl-6-iso-propylphenol: Correlation with quinone methide reactivity.  Chem Res Toxicol, 15:1106-1112.

Mimica-Dukic N, Bozin B. (2008) Mentha L. species (Lamiaceae) as promising sources of bioactive secondary metabolites. Curr Pharm Des, 14(29):3141-50.

Olsen, P., Meyer, O., Wurtzen G.  (1986)  Carcinogenicity study on butylated hydroxytoluene (BHT) in Wistar rats exposed in utero.  Food Chem Toxicol, 24:1-12.

Sun, Y., Dwyer-Nield, L.D., Malkinson, A.M., Zhang, Y.L., Thompson, J.A.  (2003)  Responses of tumorigenic and non-tumorigenic mouse lung epithelial cell lines to electrophilic metabolites of the tumor promoter butylated hydroxytoluene.  Chem Biol Interact, 145:41-51.

Umemura, T., Kodama, Y., Hioki, K., Inoue, T., Nomura, T., Kurokawa, Y.  (2001)  Butylhydroxytoluene (BHT) increases susceptibility of transgenic rasH2 mice to lung carcinogenesis.  J Cancer Res Clin Oncol, 127:583-590.

Whysner J, Williams GM. (1996) Butylated hydroxyanisole mechanistic data and risk assessment: conditional species-specific cytotoxicity, enhanced cell proliferation, and tumor promotion. Pharmacol Ther;71(1-2):137-51.

Witschi HP. (1986) Enhanced tumour development by butylated hydroxytoluene (BHT) in the liver, lung and gastro-intestinal tract. Food Chem Toxicol;24(10-11):1127-30.

Yamamoto, K., Tajima, K., Okino, N., Mizutani, T.  (1988)  Enhanced Lung Toxicity of Butylated Hydroxytoluene in Mice by Coadministration of Butylated Hydroxyanisole .  Res Comm Chem Pathol Pharmacol, 59(2):219-231