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PubMed1976

Nutritional problems in the African region.

Energy-calorie malnutrition (ECM) is the commonest nutritional problem in developing countries in Africa: 0.5-5% of the population under 6 years of age suffer from the severe forms and 4-40% from the moderate forms. It is possible that as many as two-thirds of the preschool children in developing countries in Africa suffer from some EPM (protein-calorie malnutrition). The recent Sahelian drought and civil wars in some countries in Africa have increased the size of the problem and the severity and prevalence of EPM in several parts of Africa. The aetiological factors of EPM in Africa include shortage of calories and protein, as well as increasing and recent tendency to abandon too early breast feeding, sensory deprivation, psychological and emotional trauma, ignorance, superstition and cultural taboos. The evidence available at the moment does not clearly indicate that effects of EPM on learning and behaviour are permanent, although the functions of the brain in the acutely malnourished child are defective. Malnutrition impairs immunological capability and surveillance, and hence augments the mortality and morbidity of infections such as measles especially by impairing cell-mediated immunity and, to a lesser extent, synthesis of immunoglobulins. Endemic goitre (prevalence varies from 2 to 90% in various age groups) in several parts of Africa is due to either iodine deficiency (Ethiopia) or to the goitrogenic effect of cassava diet (Zaire and Nigeria). Deficiencies of vitamins A, B complex and D have been reported in several parts of Africa, albeit sporadically. Dietary intoxications include: a) aflatoxins which may be important in the pathogenesis of hepatic carcinoma, one of the commonest neoplasms in developing countries in Africa; b) chronic cyanide intoxication from cassava (manihot) food derivatives, which on circumstancial evidence seems to be an important aetiological factor of a crippling neurological disease, the tropical ataxic neuropathy in Nigeria and Tanzania; c) organophosphate insecticides. The rarity of certain diseases in the Africans may be related specifically to the African diet, especially the high fibre and low animal fat content of many of the African diets. Examples of such diseases are atherosclerosis in the non-hypertensive non-diabetic population, cancer of the large bowel, varicose veins and perhaps multiple sclerosis.

Africa↗
PubMed2000

Effect of clinoptilolite on serum biochemical and haematological characters of broiler chickens during aflatoxicosis.

Clinoptilolite (CLI, a natural zeolite) incorporated into the diet at 1.5 and 2.5 per cent were evaluated for their ability to reduce the deleterious effects of 2.5 mg total aflatoxin (AF) kg(-1)diet on broiler chickens from 1 to 21 days of age. In total 360 broiler chicks were divided into six equal treatment groups (control, AF, CLI (1.5 per cent), AF plus CLI (1.5 per cent), CLI (2.5 per cent) and AF plus CLI (2.5 per cent)). When compared with the controls, AF treatment significantly decreased serum total protein, albumin, inorganic phosphorus, uric acid, total cholesterol and the values of haematocrit, red blood cell counts, mean corpuscular volume, haemoglobin, thrombocyte counts, percentage of monocyte counts; increased values of white blood cell and heterophil counts. The addition of CLI (1.5 per cent) and CLI (2.5 per cent) to the AF -containing diet reduced the adverse effects of AF and should be helpful in a solution to the aflatoxicosis problem in poultry.

Aflatoxins↗
PubMed1993

HBsAg and aflatoxins in sera of rural (Igbo-Ora) and urban (Ibadan) populations in Nigeria.

The purpose of this study was to screen for the presence of hepatitis B surface antigen and aflatoxins in the sera of 100 non-hospitalized individuals from the rural population of Igbo-Ora and 89 non-hospitalized individuals from the urban population of Ibadan, Nigeria. Hitherto, such a study as this has not been undertaken in this environment. The proportions of hepatitis B surface antigen carriage and serum 'pathologic' levels of aflatoxins were high (47-49%, 8.2-9.0% respectively) but varied very little between the two different populations sampled. These findings indicate that determined efforts should be instituted to reduce or eliminate hepatitis B virus infection and aflatoxin contamination of high risk foodstuffs from this environment.

Adolescent↗
PubMed1992

Efficacy of hydrated sodium calcium aluminosilicate to reduce the individual and combined toxicity of aflatoxin and ochratoxin A.

A 2 x 2 x 2 factorial arrangement of treatments consisting of dietary aflatoxin (3.5 micrograms/g), ochratoxin A (2.0 micrograms/g), and hydrated sodium calcium aluminosilicate (HSCAS, .5%) was used to evaluate the individual and combined effects of these treatments. There were six replicate pens of 10 broilers per pen for each of the eight treatments. The broilers were maintained on these treatments from 1 day to 3 wk of age with feed and water available for ad libitum intake. Aflatoxin and ochratoxin A each significantly decreased body weight, serum protein, albumin, and cholesterol and increased the relative weight of the liver, kidney, and proventriculus. Aflatoxin increased the relative weight of the heart and decreased serum aspartate aminotransferase activity and ochratoxin A increased serum uric acid. The toxicity resulting from the combination of aflatoxin and ochratoxin A was more severe than when either of these mycotoxins were present alone. Addition of HSCAS alone did not alter any of the parameters evaluated. The HSCAS reduced the toxicity of aflatoxin, but had little effect on either the toxicity of ochratoxin A alone or the toxicity resulting from the combination of aflatoxin and ochratoxin A.

Aluminum Silicates↗
PubMed1989

Prevention of aflatoxicosis by addition of hydrated sodium calcium aluminosilicate to the diets of growing barrows.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCAS/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Silicates↗
PubMed1976

[Effects of the environment on the liver and gastrointestinal tract].

The liver has a central role in the detoxication and elimination of toxic substances which enter the body as lipid-soluble compounds. Their transformation into polar watersoluble metabolites, termed biotransformation, is bound to the membranes of the smooth endoplasmatic reticulum. The oxidating enzyme in biotransformation can be induced by certain toxins and drugs. The chronic induction of enzymes by DDT and the consequences of this process of adaptation, particularly in regard to the metabolism of calcium is discussed. The protective effect of biotransformation and induction of enzymes against carcinogens, especially aflatoxin, are briefly reviewed. As examples of the chronic influence of vasotoxic substances, mention is mode of the veno-occlusive disease caused by the alkaloid phlorrhizidin found in plants, and the vinyl-chloride disease occurring in workers handling PVC. The first leads to portal hypertension of the post-sinusoidal type, while the second leads to pre- or intrasinusoidal portal hypertension and, after years of exposure, to hemangioendotheliosarcoma of the liver. The same tumor has been observed after arsenic intoxication. Arsenic may also lead to non-cirrhotic portal hypertension. The present opinions about environmentally induced gastrointestinal diseases are widely hypothetical. The high frequency of gastric carcinoma in Japan. and the varying occurrence of carcinoma of the colon in the civilized world in comparison with the rural population of tropical regions, is emphasized. The explanation for these facts is probably to be sought in differences of nutrition.

Adaptation, Physiological↗
PubMed1999

Dietary clay in the chemoprevention of aflatoxin-induced disease.

Aflatoxins are harmful by-products of mold growth and, though invisible to the naked eye, are potentially fatal. The aflatoxin problem is long-standing and inextricable. Concerns about the aflatoxins originate from the strong implications of their involvement in disease and death in humans and animals, yet scientists and clinicians are still seeking ways to effectively deal with these dangerous and elusive chemicals. Safe, practical, and effective strategies for the detoxification of aflatoxin-contaminated food and feed are highly desirable. A simple and effective approach to the chemoprevention of aflatoxicosis has been to diminish or block exposure to aflatoxins via the inclusion of HSCAS clay in the diet. HSCAS clay acts as an aflatoxin enterosorbent that tightly and selectively binds these poisons in the gastrointestinal tract of animals, decreasing their bioavailability and associated toxicities. Further studies to delineate the molecular mechanisms of action have shown that the dicarbonyl system of aflatoxin is essential for tight binding by HSCAS. In these studies, adsorption data was fitted to multiple isotherm equations including the Langmuir, multi-Langmuir, general Freundlich, Langmuir-Freundlich, Toth and various transforms. Information derived included: the Gibbs standard free energy change of adsorption, enthalpy of adsorption, capacity, affinity, and heterogeneity coefficient. Computer modeling was also utilized to provide additional structural information and insight into the mechanism. Evidence suggests that aflatoxins may react at multiple sites on HSCAS particles, especially the interlayer region, but also at edges and basal surfaces. Since clay and zeolitic minerals comprise a broad family of functionally diverse chemicals, there may be significant hidden risks associated with their indiscriminate inclusion in the diet. All aflatoxin binding agents should be rigorously tested, paying particular attention to their effectiveness and safety in aflatoxin-sensitive animals and their potential for interactions with critical nutrients.

Aflatoxins↗
PubMed1982

Field cases of aflatoxicosis in pigs.

Five cases of aflatoxicosis in pigs in southern Queensland are described. One peracute case where aflatoxin concentrations of up to 5000 micrograms aflatoxin B1/kg were demonstrated in stomach contents was presumed to be caused by consumption of mouldy bread. High levels of toxins were also present in the livers. Two cases of acute toxicity were caused by feeding mouldy peanut screenings containing 22000 micrograms aflatoxin B1/kg. One case of subacute and one of chronic toxicity were caused by sorghum grain based rations with lower aflatoxin levels (4640 and 255 micrograms/kg). Peracute toxicity caused collapse and deaths within several hours, acute toxicity caused deaths within 12 h and with subacute toxicity deaths occurred after 3 weeks on a toxic ration. Anorexia and ill thrift affecting only growing animals were seen with chronic toxicity. Extensive centrilobular liver necrosis and haemorrhage occurred with peracute toxicity and in cases of acute poisoning there was hepatic centrilobular cellular infiltration, hepatocyte swelling and bile stasis. With subacute toxicity hepatocyte vacuolation together with bile stasis and bile ductule hyperplasia were seen.

Animals↗
PubMed1981

Enhanced susceptibility to aflatoxin B1 toxicity in weanling mice pretreated with carbon tetrachloride.

Weanling male mice with or without prior treatment with CCl4 (0.5 ml/kg) were exposed to either single (20.5, 25.6, 32 and 40 mg/kg) or multiple (4 mg/kg for 10 days or 8 mg/kg for 5 days) doses of aflatoxin B1. Evidence of its acute toxic and carcinogenic effects was found only in CCl4 pre-treated mice. Single dose LD 50 value under these conditions was calculated to be 26.8 mg/kg. Histological changes which predominantly occurred in the liver were characterized by acute necrosis and degeneration of the parenchymal cells. Hepatomas were observed as early as 9 months of age in CCl4 pre-treated animals given 4 mg/kg aflatoxin daily for 10 days. It is thus suggested that the repeated use of CCl4 as an anthelmintic in animals which are apparently resistant to the lethal and hepatocarcinogenic action of aflatoxin might increase their sensitivity to this mycotoxin.

Aflatoxin B1↗