No animal species is known to be immune to the acute toxic effects of<unk> s. Adult humans have a high tolerance for<unk>  exposure and rarely succumb to acute<unk> osis, but children are particularly<unk> fected, and their exposure can lead to stunted growth and delayed development, in addition to all the symptoms mentioned below. High-level<unk>  exposure produces an acute hepatic necrosis (acute<unk> osis), resulting later in cirrhosis or carcinoma of the liver. Acute liver failure is made manifest by bleeding, edema, alteration in digestion, changes to the absorption and/or metabolism of nutrients, and mental changes and/or coma. Chronic, subclinical exposure does not lead to symptoms so dramatic as acute<unk> osis. Chronic exposure increases the risk of developing liver and gallbladder cancer, as<unk>  metabolites may intercalate into DNA and alkylate the bases through epoxide moiety. This is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis (programmed cell death). These mutations seem to<unk> fect some base pair locations more than others, for example, the third base of codon 249 of the p53 gene appears to be more susceptible to<unk> -mediated mutations than nearby bases. As with other DNA-alkylating agents,<unk>  B1 can cause immune suppression, and exposure to it is associated with an increased viral load in HIV positive individuals. The expression of<unk> -related diseases is influenced by factors such as species, age, nutrition, sex, and the possibility of concurrent exposure to other toxins. The main target organ in mammals is the liver, so<unk> osis primarily is a hepatic disease. Conditions increasing the likelihood of<unk> osis in humans include limited availability of food, environmental conditions that favour mould growth on foodstuffs, and lack of regulatory systems for<unk>  monitoring and control. A regular diet including apiaceous vegetables, such as carrots, parsnips, celery, and parsley may reduce the carcinogenic effects of<unk> . There is no specific antidote for<unk> osis. Symptomatic and supportive care tailored to the severity of the liver disease may include intravenous fluids with dextrose, active vitamin K, B vitamins, and a restricted, but high-quality protein diet with adequate carbohydrate content. In other animals In dogs,<unk>  has potential to lead to liver disease. Low levels of<unk>  exposure require continuous consumption for several weeks to months in order for signs of liver dysfunction to appear. Some articles have suggested the toxic level in dog food is 100–300 ppb and requires continuous exposure or consumption for a few weeks to months to develop<unk> osis. No information is available to suggest that recovered dogs will later succumb to an<unk> -induced disease. Turkeys are extremely susceptible to<unk> osis. Recent studies have revealed that this is due to the efficient cytochrome P450 mediated metabolism of<unk>  B1 in the liver of turkeys and deficient glutathione-S-transferase mediated detoxification. Some studies on pregnant hamsters showed a significant relationship between exposure of<unk>  B1 (4 mg/kg, single dose) and the appearance of developmental anomalies in their offspring. In 2005, Diamond Pet Foods discovered<unk>  in a product manufactured at their facility in Gaston, South Carolina. In 23 states, Diamond voluntarily recalled 19 products formulated with corn and manufactured in the Gaston facility. Testing of more than 2,700 finished product samples conducted by laboratories confirmed that only two date codes of two adult dog formulas had the potential to be toxic. In December 2020 and January 2021, Midwestern Pet Foods recalled dog food that contained fatal levels of<unk> . As many as 70 dogs had died from<unk>  poisoning by January 12, 2021.
Aflatoxin
Phoratoxin
Bukatoxin
Amatoxin
Eoxin
Ciguatoxin
Agitoxin
Toxin