To sustain life, different types of dietary constituents are required for growth, maintenance, tissue repair, and reproduction, and foods are the vehicles for them. The basic nutrient intakes exceed the requirements can lead to a variety of toxic effects. We have checked such potential adverse effects of three common dietary constituents, amino acids, fatty acids and metals. In very high intake of these three nutrients may cause pathological effect and deterioration of health. Amino acids and some metals in therapeutic dose can lead to adverse effects.
Food is an essential source of energy, building materials and nutrients. It also contains some compounds that may potentially evoke greater or lesser health disorders. Toxins can originate from the raw material or invade during processing, transportation and storage. They can be intentionally added in the form of harmless food preservatives or health promoting functional ingredients that can become toxic in combination or under environmental stressors.
Some amino acids have deleterious effects on the organism when they are present in excess amount. Adverse effects of therapeutic dose include headache, nausea, mild gastric distress, weakness, numbness over the back of the neck and the back and febrile reaction. Amino acid toxicity can be described as toxic effects on the cells of an inherited amino acidopathy with amino acid accumulation or some kind of inborn error in metabolism of amino acids.
Scriver (1995) introduced such example of inborn error of metabolism of phenylketonuria which is due to either deficiency of phenylalanine hydroxylase or deficiency of the enzyme synthesis.
Maple syrup urine disease is another example of amino acid toxicity. It is also called as branched chain ketoacidemia because it results from a deficiency of the branched chain ketoacid dehydrogenase which is responsible in catabolism of all three branched amino acids, e.g. Leucine, isoleucine, valine.
The sodium salt of glutamate- monosodium glutamic acid (MSG) has long been used as a flavour enhancer in meet products and in commercially processed foods. That causes palpitation lasting up to 2 hours is commonly called as Chinese restaurant syndrome associated with eating of Chinese food. MSG and other acidic amino acids produced lesions in retina, in accurate nucleus of hypothalamus and other brain areas devoid of blood-brain barrier and in lateral geniculate nucleus also.
The protein, gluten is found in certain cereal grains including wheat and barely rye and oats, is responsible for small bowel mucosal injury, called as
glutenenteropathy. The direct contact between the mucosa and the gluten results in cell mediated immune response or Inflammatory response in mucosa. The clinical symptoms of this syndrome are diarrhoea, weight loss, vomiting, weakness, abdominal distention, flatulence. The disorder has its onset in early childhood but the presentation of symptoms may be delayed until old age and the only treatment of this syndrome is permanent withdrawal from the diet of all foods and drugs containing gluten.
Genetically deficiency of glucose-6-phosphate dehydrogenase (G6PD) can result from broad beans and is called as favism. The amino acid, 3.4-dyhyroxypheneylalanine has capacity in vitro to lower the reduced glutathione, content of RBC, which causes jaundice, haemolysis and hemoglobinurea. The probable way to lower the risk of favism in that population appears to be through genetic breeding to reduce the glycoside, content of cotyledons.
Fatty acid toxicity
Among the all fatty acids, the erucic acid which accounts for as much as 50 % of fatty acid content of rapeseed and mustard oil (Brassica species) is the most important. The use, worldwide production of rapeseed and mustard seed oils in margarine and their important role in farming in certain countries like, India, Canada and northern Europe demands for further studies on this area. The experiments held on animals showed blockage of
β-oxidation of the fatty acid in mitochondria.
The other potentially harmful fatty acids are trans isomers of fatty acid which are consumed form variety of sources. The average intake of trans fatty acids are about 3% of total energy that includes household shortenings, margarines, spreads, dressings, fats and oil used in food products (snakes, cookies, crackers, bread, cake, potato chips, French fries), meat and dairy products. Lauric acid, myristic acid, palmitic acids and the trans fatty acid are implicated in function of cell membrane in humans and the also increase the risk of coronary heart disease (CHD).
Some other types of fatty acids also showed physiological effects even in very low concentration also. The examples of such fatty acids are epoxy oils in soybean, sunflower seed oil, cyclopropane fatty acid in oil, acids found in some species of edible fish and furanoid fatty acid.
Toxic metals
Agricultural and industrial uses of metal products posse food contamination associated with their use, storage or improper handling. The food borne metal toxicity is generally occurs after long term of consumption or children consumption at higher risk than adults. We have included only the general metal of food those are necessary as a dietary constituent.
Iron
Iron is the necessity content of the body but excess iron causes various toxic effects if accumulated in human tissues. Liver is the major storage organ of the excessive amount of iron, that's why during iron overload experiments in animals. While in humans cardio toxicity is the major effect of iron overload. Iron has also catalytic action in reactive oxygen generation, so its toxicity may be the oxidative damage caused. Experiments marked the catalytic effects of iron to be involved in carcinogenic action of polyhalogenatd aromatic hydrocarbons.
Some redox reactions, when not properly modulated by antioxidants or iron binding proteins, can damage cellular components such as fatty acids, proteins and nucleic acid. Many health disorders are related to short or long term exposure to iron in amounts exceeding the physiological capacity to protect against its reactivity. These pathological conditions range from acute iron poisoning to organ damage due to chronic iron overload. The most pronounced local effect of the iron poisoning is hemorrhagic necrosis of GI tract, manifested by vomiting and bloody diarrhoea. Systemic effects include coagulation defects, metabolic acidosis and shock.
The most common form of chronic iron overload is hereditary hemochromatosis, a genetic defect in regulation of iron absorption. The other forms of iron overload are either excessive oral iron intake or blood transfusion.
Copper
Copper is an essential nutrient needed for functions of many important enzymes and electron transporters. In blood plasma it is bound to ceruloplasmin which catalysis the oxidation Fe+2 to Fe+3. This reaction is of great physiological significance since it is only the Fe+3 form in blood that is transported by the transferring protein to the iron pool in the liver. Excess intakes of copper that cause acute or even chronic toxic effects are rare. Nevertheless, there has been instance when children accidentally ingested copper sulphate used as a pesticide on the certain crops and when there has been more chronic excess intake as in the case of "Indian childhood cirrhosis" (Barrow and Taner, 1988).
Acute symptoms of copper poisoning include nausea, headache, vomiting, diarrhea, weakness and dizziness. In more severe cases, tachycardia, hypertension and coma may occur and may be followed by jaundice, hemolytic anemia, uremia, hemoglobinurea and death.
A special form of copper toxicity occurs in Wilson's disease, a rare genetic disease associated with excessive accumulation of copper in liver, kidney, brain and cornea. Toxic manifestation of this disease can derive from normal dietary intake levels of copper (2-5 mg daily) but are accelerated by larger intake levels.
Copper accumulation leads to cirrhosis of the liver, brain and kidney damage, with brown and green corneal rings called Kayser-Fleischer rings. Wilson's diseases is fatal unless treated with copper-chelating agents to remove the copper from tissue and promote urinary excretion.
The most toxic effects of copper result from production of oxygen radicals by copper chelates, such as when ascorbate reduces Cu+2. This incoming dietary copper comes in liver and causes scar tissue to form, leading to changes in tissue architecture and reduction in liver function. Then by scarring other tissues and damage to cell membranes in kidney tubules and erythrocytes, it leads to cell lysis and connective tissue deposition.
Cobalt
In human body, cobalt serves its nutritional function as a component of vitamin B12 and its nutritional value must also be ingested as vitamin B12. The total content of cobalt inside the body is 1-2 mg. The deficiency problem with cobalt is pernicious anaemia.
Cobalt toxicity is impossible through normal diets because of small amount found in food. But in heavy beer drinkers, cobalt toxicity is identified with several instances of severe cardiac failure. In beer, cobalt salt is added in 1-2 ppm amount as a foam stabiliser. So in many cases polycythemia, thyroid epithelial hyperplasia, neurological abnormalities and pericardial effusion also developed in individuals who drink large amount of beer.
Silicon
Silicon is essential nutrient for higher animals including humans. The silicon content of the body is approximately 1g. and the normal intake in food amounts to 21-46 mg/day. Silicates are food additives used as anticaking or antifoaming agents. The toxicity of silicic acid
Is apparent only at concentrations >100mg/kg body weight.
Zinc
Zinc is an important component of a number of enzymes (e.g. lactate dehydrogenase, carboxypeptidases A and B, carbonic anhydrase, alcohol dehydrogenase. Zinc has important roles in both protein and carbohydrate metabolism. The total zinc content in the adult human is about 2-4g. Body needs zinc as a regular dietary intake, especially in periods of rapid growth. Zinc is widely distributed in many different foods.
Zinc should be considered a relatively non-toxic micronutrient in moderate supplementation levels. But the acute zinc toxicity results in gastric distress, nausea and dizziness. While in chronic toxicity gastric problems, reduction in immune function and HDL cholesterol level occurs with very high supplement.
Manganese
The functions of manganese are as a constituent of metalloenzymes and an enzyme activator. For manganese-activated reactions, the metal can act by binding either to the substrate or directly to the protein, resulting in confirmation changes.
The body contains a total of 10-40 mg of manganese. The daily requirements for this mineral are easily met by normal daily food intake.
Manganese toxicity represents a serious health hazard and results in severe abnormality of the central nervous system. In its more severe forms, manganese toxicity can result in a syndrome characterised by severe psychiatric symptoms, violent acts, hallucination, incoordination. The toxicity results in a permanent cripping of the extrapyramidal systems, the morphological lesions of which are similar to those of parkinson's disease. There have been number of cases of manganese toxicity in individuals who consume water containing high manganese concentrations.
Conclusions
Other food borne toxicants
Besides amino acids and fatty acids, other sources of plant origin like alkaloids, estrogens, lipids, lectines, enzyme inhibiters, saponins are also have some toxic effects. While there are a lot of other food additives which may lead to some poisonous effects. Food additives include food colours, packaging materials, flavour enhancers, surface active agent, emulsifier, should be checked for their toxic effects. Pesticides and carcinogens and mutagens in food cause severe toxic effects. More affected food contaminants are microbial agents, those includes bacterial toxins, fungal toxins and mycotoxins are major cause of common food born illness.
Food toxicology differs from other types of toxicology because of the nature and chemical complexity of food. The law and regulation of food safety provides workable scheme for establishing the safety of foods.
