Organoleptic and laboratory methods for determining meat from dead, agonized, and sick animals. The reaction to peroxidase is positive. The reaction to peroxidase in animal meat.
The essence of the reaction is that the peroxidase enzyme found in meat decomposes hydrogen peroxide to form oxygen, which oxidizes benzidine. In this case, paraquinone diimide is formed, which with underoxidized benzidine gives a compound (paraquinone diimide) of a blue-green color that turns brown.
During this reaction, peroxidase activity is important. In the meat of healthy animals it is very active; in the meat of sick animals and those killed in an agonal state, its activity is significantly reduced.
Peroxidase + benzidine + 2H 2 O 2 + benzidine
paraquinone diimide (blue-green color, turning into brown-brown).
Determination technique. Pour 2 ml of meat extract into a test tube in a ratio of 1:4 (prepared to determine pH using a colorimetric method), add 5 drops of a 0.2% benzidine solution, shake and add 2 drops of a 1% hydrogen peroxide solution.
Evaluation of results. At After a positive reaction, the meat extract after 0.5 - 1.5 minutes acquires a blue-green color, which quickly turns into brownish-brown. This reaction is characteristic of meat obtained from a healthy animal.
Weak positive reaction (doubtful). The extract from the meat of overworked, old and sick animals acquires a blue-green color, which with a delay turns into brown-brown.
Negative reaction. In the extract from the meat of seriously ill animals or those killed in an agonal state, the blue-green color does not appear, and the extract immediately acquires a brownish-brown tint.
6.5 Formol reaction (according to G.V. Kolobolotsky and E.V. Kiselev)
In case of severe diseases, even during the life of the animal, intermediate and final products of protein metabolism - polypeptides, peptides, amino acids, etc. - accumulate in the muscles in significant quantities. The essence of this reaction is the precipitation of these metabolic products with formaldehyde.
Determination technique. To set up the reaction, an aqueous extract from the meat being tested is required in a 1:1 ratio. To prepare a 1:1 extract, a meat sample is freed from fat and connective tissue and weighed out 10 g. Then the sample is placed in a mortar, thoroughly crushed with curved scissors, 10 ml of saline and 10 drops of 0.1 N sodium hydroxide solution are added.
The meat is ground with a pestle. The resulting slurry is transferred using a glass rod into a flask and heated to boiling to precipitate the proteins. The flask is cooled with cold water under the tap, after which its contents are neutralized by adding five drops of a 5% solution of oxalic acid and passed into a test tube through filter paper. If the extract remains cloudy after filtration, filter again or centrifuge.
Industrially produced formalin has an acidic environment, so it is first neutralized with 0.1 N sodium hydroxide using an indicator consisting of an equal mixture of 0.2% aqueous solutions of neutralrot and methylene blue until the color changes from violet to green.
For the reaction, pour 2 ml of the extract into a test tube and add 1 ml neutral formalin.
Evaluation of results. Positive reaction. The extract obtained from the meat of an animal killed in agony, seriously ill or butchered after death turns into a dense clot.
Questionable reaction. When extracted from the meat of a tired or sick animal, flakes fall out.
Negative reaction. The extract from the meat of a healthy animal remains transparent or becomes slightly cloudy.
Meat is considered to be obtained from a healthy animal if there are good organoleptic characteristics of the carcass, the absence of pathogenic microbes, pH 5.7 - 6.2, a positive reaction to peroxidase and a negative formol reaction. The meat of a sick or overworked animal is not sufficiently bled, pH 6.3 - 6.5, the reaction to peroxidase is negative, and the formol test is positive (flakes). The meat of an animal killed in a state of agony is poorly bled, with a bluish or lilac-pink color of the lymph nodes, pH 6.6 or higher, the reaction to peroxidase is negative, and the formol reaction is accompanied by the formation of a jelly-like clot.
Table 2 Laboratory parameters of meat from healthy and sick animals
|
Indicators |
Meat from healthy animals |
Meat from a tired and sick animal |
Meat from a seriously ill animal or one killed in agony |
|
1.Bacterioscopy of fingerprint smears |
There is no microflora |
Single cocci or bacteria |
There are cocci, rods |
|
2. pH of meat extract |
6.6 and above |
||
|
3. Reaction to peroxidase |
Positive (blue-green color, quickly turning into brown-brown) |
Doubtful or weakly positive (blue-green coloration with a delay, turning into brown-brown) |
Negative (the blue-green color does not appear, and the hood immediately acquires a brown-brown color) |
|
4. Formol test (for cattle meat) |
Negative (the hood remains transparent or becomes slightly cloudy) |
Doubtful (flakes fall out) |
Positive (a dense clot is formed) |
-acute myeloid leukemia
- chronic lymphocytic leukemia
+undifferentiated leukemia
- acute lymphocytic leukemia
-chronic myeloid leukemia
/\173. In the pathogenesis of disorders of the coagulation mechanism of hemostasis, it is important
-decrease in platelet count
- platelet dysfunction
-vasopathy
+ factor VIII deficiency
-defect of platelet receptors IIb-IIIa
/\174. Thrombocytopenia is characterized by
- deficiency of plasma coagulation factors
-extension of blood clotting time
- hematoma type of bleeding
+petechial type of bleeding
- bleeding time is normal
/\175. Platelet adhesion and aggregation decreases with
-excess calcium and magnesium
- deficiency of VIII f blood coagulation
-increased blood concentration of ADP
-excess thromboxane A2
+ von Willebrand factor deficiency
/\176. Hereditary deficiency of procoagulants occurs when
+ hemophilia
-vitamin K deficiency
-liver failure
-formation of antibodies to procoagulants
-impaired carboxylation of prothrombin complex factors
/\177. Hemophilia A is characterized by
-autosomal recessive type of inheritance
- deficiency of IX blood coagulation
- petechiae, ecchymoses
+hemarthrosis
-extension of bleeding time
/\178. Von Willebrand disease is characterized by
-reducing the duration of capillary bleeding
-shortening blood clotting time
-increased platelet aggregation ability
-impaired synthesis of factor VIII
+decrease in procoagulant activity of factor VIII
/\179. In the pathogenesis of hypercoagulation in DIC syndrome it is important
+ activation of “external” and “internal” blood coagulation mechanisms
-hypofibrinogenemia
-activation of the fibrinolytic system of the blood
-excess antithrombin III
-thrombocytopathy
/\180. In the pathogenesis of hypocoagulation in DIC syndrome it is important
+coagulopathy and thrombocytopenia consumption
-excess procoagulants
- entry into the blood of a large amount of tissue thromboplastin
-activation of fibrinolysis inhibitors
- antithrombin III deficiency
/\181. The most severe stage of DIC syndrome in newborns
+hypocoagulation
-hypercoagulation
-transitional
-recovery
-terminal
/\181. Clinical manifestations of hemorrhagic disease of the newborn include
+melena, bleeding from the umbilical wound
- yellowness of the skin and mucous membranes
-kernicterus
-hyperbilirubinemia
-edema
/\182. In hemophilia A,
+Formation of active prothrombinase
-Transition of prothrombin to thrombin
-Transition of fibrinogen into fibrin
-Second phase of blood coagulation
-Third phase of blood coagulation
/\183. Hypercoagulation of blood occurs when
-Excess protein C
-Excess protein S
-Excess of antithrombin-III
+Factor V resistance to protein C
-afibrinogenemia
/\184. Etiological factors of exogenous origin causing damage to the nervous system
+alcohol intoxication
-damage to neurons in hepatic coma
-cerebral ischemia
-hypoglycemia
-damage to neurons due to uremia
/\185. Through nerve conductors they enter the nervous system
-streptococcal exotoxin
-meningococci
-pneumococci
- Escherichia coli
+rabies virus
/\186. Cause of spongy transmissible encephalopathy
-Cytomegaloviruses
-Enteroviruses
-Rabies viruses
-Herpes virus
+Prions
/\187. Viruses that form intracellular inclusions in neurons
-Cytomegaloviruses
-Enteroviruses
+Rabies viruses
-Herpes virus
-Polymyelitis virus
/\188. Braking deficiency is
+ release of the underlying parts of the central nervous system from the control of the overlying parts
-reduction of neural influences on postsynaptic structures
/\189. Denervation syndrome is
-impaired transport of trophogens and formation of pathotrophogens
-decrease in afferent impulses into the neuron
- release of the underlying parts of the central nervous system from the control of the overlying parts
+reduction of neural influences on postsynaptic structures
-a group of hyperactive neurons
/\190. Primary inhibition deficit develops due to
-excessive stimulation of the nervous system
+ disorders of the structure and function of inhibitory neurons
-increasing the synthesis of excitatory mediators
/\191. Secondary inhibition deficit develops due to
+ actions of depolarizing agents of excitatory amino acids leading to excessive neuronal activity
-disorders of the structure and function of inhibitory neurons
- disturbances in the structure and function of excitatory synapses
-decreased synthesis of excitatory mediators
-excess of descending inhibitory influences during the destruction of parts of the nervous system
/\192. The consequence of disinhibition syndrome may be
-development of dystrophic changes in neurons and innervated structures
+ formation of GPUS (generator of pathologically enhanced excitation)
-development of denervation syndrome
-development of organ atrophy
-development of deafferentation syndrome
/\193. Pathologically enhanced excitation generator (PAG) is
+ an aggregate of hyperactive interacting neurons producing an uncontrolled flow of impulses
- a set of cascade membrane and intracellular processes
- a complex of changes in synaptic structures
- trophic disturbance caused by loss or change in nervous influences
A complex of changes that occur in postsynaptic neurons, organs and tissues after the loss of nervous influences on these structures
/\194. The importance of GPUV education
-promotes the formation of diffuse inhibition
+ is a determinant of the pathological system and contributes to the formation of the pathological system
-promotes the formation of the physiological system
-increases the trophic influence of the neuron on the innervated structures
-inhibits the development of neuropathological processes
/\195. Slow hyperkinesis includes
-convulsions
+athetosis
-tics
-chorea
-tremor
/\196. Neuroses can lead to the development
+ duodenal ulcer
-meningitis
- spongy transmissible encephalopathy
-encephalitis
-Alzheimer's disease
/\197. Central paralysis is characterized by:
-preservation of voluntary movements
-weakening of tendon reflexes
+increased tendon reflexes
-absence of pathological reflexes
-decreased muscle tone
/\198. Peripheral paralysis is characterized by
-increased spinal reflexes
-the appearance of pathological reflexes
- muscle hypertrophy
+muscle hypotonia
- muscle hypertonicity
/\203. Pain mediators include
-physiological concentrations of adrenaline
-enkephalins
-endorphins
+bradykinin
-dynorphin
/\204. The sensation of pain is formed in
-nociceptors
-nerve trunks
-spinal cord
-reticular formation
+ neurons of the thalamus and cerebral cortex
/\205. Most susceptible to pain
+ skin and mucous membranes
-liver
-brain
-spinal cord
-myocardium
/\206. Phantom pain is pain
-in the left arm and left shoulder blade during an attack of angina pectoris
-above the collarbone in acute hepatitis or irritation of the parietal peritoneum
- for brain diseases
+ in a missing part of the body, most often after amputation of limbs
- girdle pain with pancreatitis
/\207. In the pathogenesis of phantom pain they are important
-increased sensitivity of nociceptors
-increased conductivity of nerve trunks
-increased excitability of the cerebral cortex
Formation of amputation neuroma and the formation of a generator of pathologically enhanced excitation in the spinal cord
-inhibition of brainstem excitability
/\208.The antinociceptive system includes
-bradykinin
+gelatinous substance
-ions H, K
-histamine
-substance P
/\209.Reduced pain sensitivity when rubbing the skin and massage is due to
-decreased sensitivity of nociceptors
- blockade of nerve conductors
-decreased excitability of neurons of the reticular formation
-inhibition of the excitability of thalamic neurons
+ activation of the gelatinous substance of the spinal cord
/\211. The leading link in the pathogenesis of diabetic hyperosmolal coma is
+hyperglycemia
-ketosis
-lactic acidemia
-hypoxia
-hyperazotemia
/\212. Ischemic stroke may be caused by
+thrombosis or embolism of cerebral vessels
- rupture of a cerebral aneurysm
- cerebral vascular dystonia
- arterial hyperemia of the brain
-reduced blood clotting
/\213. The cause of hemorrhagic stroke may be
+ arterial hypertension
-stenotic atherosclerosis of cerebral vessels
-thrombosis and embolism of cerebral vessels
-angiospasm of cerebral vessels
-increased hematocrit
/\214. In ischemic stroke, in contrast to hemorrhagic stroke, the clinical picture is often dominated by
-Cerebral edema
+Focal symptoms
-Blood in the cerebrospinal fluid
-Compression of brain tissue
-Increased intracranial pressure
/\215. Cerebellar ataxia, memory impairment for current events, nystagmus, dysarthria, dysphagia, hiccups, dizziness are characteristic of damage
+Vertebral artery (posterior inferior cerebellar artery)
-Anterior cerebral artery
-Middle cerebral artery
-Posterior cerebral arteries
-Pial arteries
/\216. Paresis or spastic paralysis of the limbs (proximal arm and distal leg), loss of sensation on the side opposite to the lesion is observed when damaged
-Vertebral artery (posterior inferior cerebellar artery)
+Anterior cerebral artery
-Middle cerebral artery
-Posterior cerebral artery
-Pial arteries
/\217. Patient M., 64 years old, diagnosed with ischemic stroke, was diagnosed with a positive Babinski reflex on the left, loss of sensitivity on the left side of the body.
In the presence of hydrogen peroxide and peroxidase, benzidine forms a more complex compound of two molecules, colored blue. It gradually decomposes to form a brown substance.
The disadvantage of the benzidine reaction is its diffuse nature. To eliminate it, ammonium molybdate is added to the reagent, which precipitates the colored substance.
Reagents
1) 0.85% solution of table salt.
2) 0.1% solution of ammonium molybdate in saline solution.
3) A saturated solution of benzidine in saline.
4) 20% hydrogen peroxide solution.
5) A mixture of hydrogen peroxide and benzidine at the rate of 1 drop of hydrogen peroxide per 2 ml of benzidine (mix before use).
Carrying out the reaction
1. Place the sections in a 0.85% solution of table salt at 4°C in a watch glass for 3 minutes.
2. Treat the sections with a solution of 0.1% ammonium molybdate in saline solution for 5 minutes.
3. Treat the sections with a solution of benzidine, mixed with hydrogen peroxide before use, for 5 minutes (until a blue color appears).
4. Rinse sections with fresh, chilled saline solution.
5. Observe the localization of the blue color.
Reaction results (Tables 28, 29)
In the cabbage leaf, blue crystals fall out in places where active peroxidase accumulates. The reaction occurs in all leaf tissues with noticeable intensity, and more or less evenly throughout the entire parenchyma. In bundles, the phloem part is especially intensely colored. The cambium is much less stained. The abundance of peroxidase in the phloem is apparently explained by the fact that plastic substances moving through the cells undergo partial oxidation and are spent on the synthesis of substances of new cells formed by the cambium.
In the corn grain, the reaction occurs with insignificant intensity. In the embryo the color is almost as weak as in the endosperm. More intense color characterizes conductive elements. The coloring of the cytoplasm of the cells giving the reaction is uneven; plastids are stained much more strongly than the cytoplasm.
Organoleptic methods include determining: appearance and color; condition of the muscles on the cut; consistency; smell; transparency and aroma of the broth.
Each selected image is analyzed separately.
Equipment and materials
- · General purpose laboratory scales in accordance with GOST 24104--2001 4 with a maximum weighing limit of 200 g, permissible error of 20 mg.
- · Medical scalpel according to GOST 21240--89.
- · Medical tweezers according to GOST 21241--89.
- · Household meat grinder in accordance with GOST 4025--95 or household electric meat grinder in accordance with GOST 20469--95. Conical flask Kn-100 according to GOST 25336--82.
- Electric water bath
- · Medical scissors according to GOST 21239--93.
- · Knife.
- · Funnels according to GOST 25336--82, type VF
- · Measuring cylinders according to GOST 1770--74. with a capacity of 25, 100 cm 3.
- · Glasses according to GOST 25336--82, type B or N. with a capacity of 50 cm-".
- · Watch glass.
- · Glass rods.
- · Filter paper according to GOST 12026--76.
- · Household gauze according to GOST 11109-90.
- · Distilled water according to GOST 6709--72.
Determination of the appearance and surface of the carcass, integumentary and internal adipose tissue and abdominal serous membrane is carried out by external examination.
Determining the condition of the muscles on the cut
The thigh muscles are cut across the muscle fibers. To determine the muscle attribute, filter paper is applied to the surface of the muscle cut for 2 s.
To determine muscle stickiness, touch the surface of the muscle section with your finger. The color of the muscles is determined visually in diffuse daylight.
Determination of consistency
On the surface of the rabbit carcass in the area of the femoral muscles, a hole is formed with the lungs and the time of its leveling is monitored.
Odor detection
Preparing for the test
To determine the smell of fat, at least 20 g of internal adipose tissue is taken from each sample. Each sample is crushed with scissors, melted in beakers in a water bath and cooled to a temperature of 20 1 WITH.
GOST R 53228--2 (GOST 20235.0-74 S. 3) is in force on the territory of the Russian Federation
Carrying out the test
The smell of internal fat is determined organoleptically by stirring it with a clean glass rod.
The smell of the surface of the carcass and the abdominal cavity is determined organoleptically.
To determine the smell of the deep layers, make a cut in the mouse with a clean knife. Particular attention is paid to the smell of the layers of muscle tissue adjacent to the bones.
Determining broth clarity and aroma
Preparing for analysis
From each sample (carcass), pieces of muscle weighing 25 g each are cut out with a scalpel from the area of the thigh, shoulder blade, back, butt and chopped twice in a meat grinder.
The minced meat is thoroughly mixed and weighed.
To prepare meat broth, weigh 20 g of minced meat on a laboratory scale, place it in a conical flask with a capacity of 100 cm3 and pour in 60 cm3 of distilled hearth. The contents of the flask are thoroughly mixed. The flask is covered with a watch glass and placed in a boiling water bath for 10 minutes.
Carrying out analysis
The smell of meat broth is determined during the process of heating to 80 "C - 85" C at the moment of the appearance of vapors escaping from the slightly open flask, by sensing their aroma. The transparency of the broth is determined visually by examining 20 cm 3 of broth poured into a measuring cylinder with a capacity of 25 cm 3 and a diameter of 20 mm.
Organoleptic method
Rabbit meat (domestic) weighing 2 kg is good, no bruises were observed, no foreign odors, no blood clots, no bile stains. The smell is characteristic of this type of meat, the color is white-pink. The broth turned out transparent, without a characteristic smell, which means that the meat is fresh.
Peroxidase reaction
The essence of the reaction is that hydrogen peroxide, in the presence of the enzyme peroxidase, oxidizes benzidine, forming paraquinone diimide, which, with underoxidized benzidine, produces a blue-green compound that turns brown (color reaction). The activity of peroxidase, like any enzyme, depends on the pH of the environment. 2 ml of the extract filtrate (1:4) is poured into a test tube, 5 drops of a 0.2% alcohol solution of benzidine are added, the contents are shaken, after which 2 drops of a 1% solution of hydrogen peroxide are added. The reaction is read within 1-2 minutes.
The extract first acquired a blue-green color, then within 1-2 minutes it turned brown-brown. This analysis indicates that the meat is fresh.
