Dinatec, Inc


Dinasil is a product that is formulated to bind toxins produced by molds (mycotoxins) in such a way that it will not be absorbed by the animal.

What does Dinasil contain?

Dinasilcontains Aluminum silicate.

How does Dinasil works?

Dinasilbinds mycotoxin inside the animals digestive system allowing the mycotoxin to pass through without causing any harm.

Does Aluminum Silicates bind other minerals?

Based on studies conducted at the University of Georgia there is no nutrient binding that occurs in the animal feeds. If however binding does occur the potential is of very low magnitude and would result in only minor consequence on the animals perfor­mance.

Why do I need to include mold inhibitor in the feeds?

It is stated that molds can potentially grow starting from the field up to the house of the animals.  Once the mold grows it begins to produce mycotoxins which causes many harm to the ani­mals. A toxin binder is the only means of getting rid of these harmful toxins after they are produced in the feed.

Is it still necessary to put a toxin binder if mold inhibitor is already mixed in the feeds?

Yes. A toxin binder is specifically used to bind mycotoxins produced by molds, while a  mold inhibitor stops mold reproduc­tion.

When molds are present, toxin is consequently produced there­fore, a toxin binder is necessary.

A very effective preparation for protection against molds and toxin isDinasilPLUSwhich is  a combination of a  mold in­hibitor and a toxin binder.  This will better protect the essen­tial nutrients in feeds as well as your animals.  Mycotoxicosis is no more a worry.

How much Dinasil and Dinasil PLUS will I place in a ton of feed?

Dinasil is added at a rate of 1 kg per ton of finished feed.

Dinasil PLUS is added at 1 ‑ 2 kg in every ton of feed.


Some are carcinogenic and many are synergetic with pathogenic or disease conditions. For example there a corroborated evidence to sustain the impairment of immunity response of affected animals (Charts 2 & 3).  There is also documented synergism with coccidiosis, salmonella, (Chart 4) crop mycosis and nutritional deficiencies (Chart 5) (Poultry Science  53;721‑725, 1974 immunal suppression in chickens by aflatoxins, J.P. Faxton, H.P. Tung and P.B. Hamilton).  'The relative sizes of both the bursa of fabricious and thymus were reduced by dietary aflatoxin. The bursa decreased by approximately 1/4 at the higher doses of aflatoxins while the thymus regressed to about 1/2 of normal size'.

The study indicates that dietary aflatoxin is a potent immuno-suppressant in the young chicken and that the extent of suppression of that response is related to the dose of aflatoxin as well as the duration of the treatment.  Poultry Science 54; 1693‑1696, 1975 interaction of T2 toxin with salmonella infections of chickens.  Boon Bungearn Boonchuvit, P.B. Hamilton and  H.R. Burmeister 'The interaction demonstrated  between T2 toxin and para typhoid infections which manifest themselves as increased  mortality, has important implications for the  poultry industry' (Chart 4).

The  severity of mycotoxicosis will probably vary widely and  any of the following parameters will have a marked influence . Things such  as level in the substrate, condition of litter, age of livestock, ex  of livestock, genetic compliment, environment, temperature, humidity,  the state of nutrition, the state of production and presence of other diseases (Chart 6). One well known kind of mycotoxin is called aflatoxin.  Aflatoxicosis is the related problem to the aflatoxin  generating types of molds.  Aflatoxins have received more attention in the last few years, this is mainly due to feed or litter infection in poultry. It is known to be responsible for poor feed conversion and  loss of egg production.   Aflatoxins have the following etiology.

There are several types ‑ B1 ‑ the most important in poultry.  B2, G1, G2, M1 and M2 which are related to dairy cattle and others(8).  Aflatoxins are produced by aspergillus flavus and Aspergillus Parasiticus and some species of penicillia.  The substrate can be found in corn, barley, millet, peanut peas, rice, sorghum, wheat, coastal hay and oats.  Smith and Hamilton Poultry Science 49; 207‑215, did a study which centered around the percent positive feed ingredients for aflatoxin taken from several sources.  The study indicated an ascending level of positive incidence with aflatoxin content going from 0%, soybean meal 5%, corn 30%, feed from the mill 52%, and  feed from the trough at 91% positive rate.  This is quite important.  These troughs had a high concentration of positive results when tested for aflatoxins.


Mold  problems are enhanced throughout the feed  chain  process starting with harvest, the problems related to  excessive handling, inadequate drying, holding too long before drying without ventilating, improper storage and  cleaning, moisture buildup in bins from leakage, from lack  of aeration, insect damage in storage, poor sanitation, and poor clean up of bins and feeders.  There are many things that are related to mold contaminated feed and its effects on livestock performance. Some of the most important ones can be summarized as depressed weight gain  and reduced feed efficiency.  For layers we find  decreased feed  intake  and  drop in egg production, on broilers  there is  decreased carcass quality as well.

North Carolina State University conducted a study which shows that the amount of #1 quality carcasses decreased from 59.6% To 28.8% When comparing a group of broilers which had been treated with anti‑molding solutions  (See Chart 8) the external symptomatology of mycotoxicosis problems can be summarized as  follows:  in the poultry industry you  will  find increased  morbidity, increased mortality, a higher percentage of deformed  legs.  In the processing plant increased bruising (See Chart  9) both inside and outside of the skin layers, Drs. Tung, Smith, and Hamilton corroborate the effects of aflatoxicosis on bruising in the chicken in their paper #3248 of the journal series of the North Carolina State  University Agricultural Experiment Station in Raleigh, North Carolina, in which they state 'the finding that aflatoxin can make chickens more susceptible to bruising has significance to the poultry industry since  bruising results in condemnation losses of several million broilers every year.  The introduction of  susceptibility  to bruising by  doses of aflatoxin too small to inhibit growth  and the occurrence of this condition within 48 hours after the aflatoxin is incorporated into the diet indicate the insidiousness  of aflatoxicosis and the difficulty of  diagnosing and controlling it.'

Intestinal fragility during ochratoxicosis and aflatoxicosis has been  demonstrated by Drs. Warren and Hamilton in their paper 6132 of the journal series of the North Carolina State University Agricultural  Experiment Station in Raleigh, North Carolina.  Ochratoxins were found to debilitate the intestinal wall.  Post mortem lesions associated with mycotoxicosis include but are not limited to the following:  pale yellow fatty livers and distended gall bladders, congested kidneys usually enlarged, hemorrhaging of muscles and  viscera, regressed bursa of fabricious and thymus, enlarged spleen and pancreas, hydropericardium and acetis pale bone marrow.

In  problems related to aflatoxicosis the target organ is the liver and the most sensitive metabolic systems are protein synthesis,  lipid synthesis and lipid transport. Increased lipid content of the liver has been substantiated and has been observed to  increase from 30% to over 60% in as many as  10  parts  per million content of aflatoxins.  (See Chart 10).  Bone  strength of livestock also is affected.  Drs. Hoff, Doerr, Hamilton, Hamann, Peterson and Ziegler in their paper titled  'Evaluation of bone strength during aflatoxicosis and ochratoxicosis', conclude that aflatoxin and ochratoxin have debilitating effects on bone properties.  The breaking strength, of the bones, was decreased and the flexibility of the bones was increased. Gizzard erosion, crop mycosis, oral lesions caused by ingestion of dietary fusariotoxin have been documented by Drs. Wyatt, Weekes, Hamilton and Vermyster (See  Applied  Microbiology  August 1972 pages 251‑257).  Also documented has been the interference  with pigmentation or carotenoid metabolism during ochratoxicosis in young broiler chickens.


In addition to the problems related to poultry, mycotoxicosis is a  dangerous entity for other livestock farmers.  It has been substantiated that milk  production by dairy cattle can be reduced  drastically by mycotoxicosis. This phenomenon may not be due directly to the mycotoxicosis effect but the result of the cattle consuming less feed normally within 12 hours of consumption of aflatoxin, for example, with the resulting  decreased milk production 2 days later.

The following is a summary of the symptoms of aflatoxicosis in dairy cows which have been observed in nine different studies by Mertens, D.  R., 1979.  'Biological  effects of mycotoxins upon rumen function and lactating dairy cows.  In; ' Interactions of mycotoxins in animal production' PP. 118‑136.  National Academy of Science U.S.A., Washington, D.C.:


  • Unthriftiness,  lethargy  and anorexia.
  • Decreased milk production
  • Normal or below normal body temperature.
  • Dry peeling skin on the muzzle.
  • Prolapse of the rectum.
  • Liver damage including  bile, ductile proliferation, necrosis diffuse fibrosis, inflammation
  • of the veins and arteries, fatty infiltration
  • Elevated blood levels of cholesterol, bilirubin, and the enzymes aspartate and
  • aminotransferase. Lactic dehydrogenase and alkaline phosphates.
  • Edema of the abdominal cavity.

We know many of these findings are not necessarily specific for aflatoxicosis therefore making a diagnosis becomes that much more difficult.  Added to this problem is the fact that with ruminants it is very  difficult to say whether the toxin in  question  is causing  a  malfunction  of the rumen or a  systematic  toxicity.

This is particularly true with certain types of mycotoxins which can  have a very strong anti‑microbial activity. We know from both 'in vitro' and 'in vivo' studies that aflatoxin  impairs  rumen  function by decreasing cellulolysis, production of volatile fatty acids and ammonia and by altering the proportions of the volatile fatty  acids  produced.  One very important area to look at with  dairy cattle is the possibility of toxic residues occurring in the products consumed by humans.  This is particularly important with lactating  cows which may excrete mycotoxins or their metabolites in milk.  Since milk is a major component in the diet of babies and children, and as the young of any given species are much more susceptible to this problem than adults this becomes a paramount problem  for the livestock farmer and the marketing sectors to deal with.  Mr. Armbrecht et al.  Reports his finding upon giving sows feed containing 100 parts per billion of aflatoxin and found that from these 1.5 parts per billion were found in the milk and 8 parts per billion were located in the livers of the nursing pigs.

In dairy cattle there was a linear relationship between intake and excretion in milk which correlates to 1% of the intake being excreted as a toxic metabolite of the incoming aflatoxin.

Mycotoxins also cause a severe problem in the swine industry. F‑2 toxin (Zearalenone) for example has been known to cause a number of  problems:  among these infertility, false  heat, hyperestrogenic  activity  and in some very sensitive  animals, like pigs,  this F‑2 toxin can produce also  swollen edematous vulva and vaginal prolapse in addition an enlarged  uterus  and atrophy of the ovaries can be observed.  Ovulation is hindered by the oocytes that can die in the graafian follicle.  Because of the fact that the uterine glands in the mucosa of the  uterus degenerate, ovulation and fertilization  become  difficult to maintain.  You  will also observe in male pigs atrophy  of the testes and the development of the mammary glands  evident.

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