Study on the toxicity and application of sodium p-aminophenylarsinate_Kain Industrial Additives

Background and overview[1][2]

Sodium p-aminophenylarsinate is also called asanic acid (p-ASA). As an organic arsenic feed additive, it is widely used in the breeding industry to promote animal growth. The absorption and transformation efficiency of p-ASA in animals is low, and most of it is excreted as prototype (Morrison, 1969) and directly enters the farm soil and water.

Toxicity studies[4]

P-Aminophenylarsonic acid (P-ASA) is widely used as a feed additive for livestock and poultry due to its anti-coccidial and antibacterial effects. However, in recent years, it has been found to remain in animals and in their feces. The problem of environmental pollution through urinary excretion has become increasingly prominent. Zhang Qian took advantage of the small particle size and sufficient absorption of nanoparticles to process p-aminophenylarsonic acid into nanoparticles (P-Arsanilic Acid Nanoparticles, P-ASAP) and found out: Compared with P-ASA, P-ASAP has good growth-promoting properties and has lower arsenic residues in the liver and feces, but its safety is unknown. Without safety, there will be no market. For this reason, this article conducted P-ASAP Acute and subacute toxicity tests. Test 1. Acute toxicity test: 36 SD rats (half female and half male) were randomly divided into 6 groups. The pre-test was 7 days. On the 1st day of the formal test, groups Ⅰ, Ⅱ, Ⅲ, Ⅳ, and Ⅴ were divided into 6 groups according to the weight per kg body weight. P-ASAP 400 mg, 588 mg, 864.36 mg, 1270.6 mg and 1867.8 mg were orally administered once. The control group was orally administered the same dose of normal saline. The fixed volume dilution method was used to prepare the oral solution. The patients were observed for 14 days and the incidence and incidence rates were calculated. Mortality rate, calculate its median lethal dose (LDso). Test 2. Subacute toxicity test: 112 SD rats (half female and half male) were randomly divided into 7 groups: P-ASA and P-ASAP were added according to 1/5, 1/50 and 1/100 of their respective LDso. In the feed, the control group was not added. The pre-feeding period was 7 days, and the formal test was 36 days. Weigh every week, observe clinical symptoms and perform pathological anatomy of dead rats. On the 18th and 36th day of the experiment, 6 rats from each group were randomly selected and culled, and the internal organs were removed for pathological and histological examination; serum was collected to detect: (1) liver function (2) renal function (3) oxygen free radical levels and anti- Oxidase activity; (4) Take liver and feces to detect the content of arsenic (AS5, AS3, MMA, DMA) in different valence states. The results are as follows: Test 1. Acute toxicity test: The LD5o of P-ASAP is 765.036 mg·kg-1, and its 95% confidence limit is 561.5 mg·kg-1 ~ 1006.95 mg·kg-1. Test 2. Subacute toxicity test: 1. Body weight, morbidity and mortality 18 days and 36 days, the body weight of the medium and low dose groups of P-ASAP and P-ASA were extremely significantly higher than that of the control (P0.05), the values ​​of T-BIL, ALP and AST in the P-ASA group were lower than those in the P-ASAP group, and The difference in ALT was significant (P<0.05). 4. Renal function 18 and 36 days, BUN and Cr, BUN and Cr in each P-ASA group were higher than those in the control group, P1 difference was significant (P<0.05), BUN, Cr in each P-ASA group were higher than those in the corresponding P-ASAP group Cr is high (P<0.05). 5. Oxygen free radical levels and antioxidant enzyme activity SOD, 18d and 36d, compared with the control group, as the exposure dose increased, the SOD activity of each group of P-ASAP and P-ASA increased, among which P1 was significantly higher than P3 (P<0.05). GSH-Px, on 18d and 36d, the GSH-Px activity of each P-ASAP and P-ASA group was extremely significantly lower than that of the control group (P<0.01). Except for the medium-dose group, the GSH-Px activity of each P-ASAP group were respectively higher than the corresponding P-ASA groups, (P<0.05). MDA: On 18d and 36d, the MDA levels of each group increased with the increase of the poisoning dose, and were extremely significantly different from the control group (P0.05), among which the contents of NK and P1AS3 were significantly different (P <0.05); the DMA and MMA contents in each group were higher than those in the control group, and increased with the increasing dose of poison. Among them, the DMA in group P1 increased significantly (P<0.01). 7. The contents of arsenic in different valence states in the liver, AS3 and 18d, were higher than those in the control group, and increased with increasing doses of poisoning. Except for the AS5 contents in the N2, N3, and P3 dose groups at 18d and 36d, each level was higher than that in the control group. The contents of AS3 and AS5, DMA and MMA in the test group were all higher than those in the control group. The AS3 contents in the P1 and P2 groups were extremely significantly (P<0.01) and significantly (P<0.05) increased respectively. Among them, the DMA content in N1 and P1 groups increased significantly (P<0.01) and significantly (P<0.05) respectively. The conclusion is that compared with P-ASA, P-ASAP has greater hepatotoxicity than P-ASA, and has less nephrotoxicity, oxidative toxicity and intrahepatic valent arsenic toxicity than P-ASA.

Applied Research[3]

144 “Changjia (Xing)” hybrid pigs were divided into 4 groups according to weight, gender and genetic basis (each group had 3 replicates, 12 pigs in each replicate), and were fed with p-aminophenylarsonic acid (PAPAA)-free ) (Group 1) and the same corn-soybean meal type diet supplemented with 70mg/kgPAPAA (Group 2), 70mg/kgPAPAA +70mg/kgOTC (Group 3) and 70mg/kg PPAAA +70mg/kgCTC (Group 4). The results showed that the daily weight gain of groups 2, 3 and 4 increased by 8.7% (P <0.05), 13.6% and 14.6% (P <0.01) respectively; the feed conversion rate increased by 11.5% and 15.4% respectively. % and 15.0% (P <0.0 1). The carcass fat rates of groups 2 and 3 were reduced by 16.5% and 14.5% respectively (P <0.01); the backfat thickness of group 2 was reduced by 16.3% (P <0.01), the lean meat rate increased by 6.7% (P <0.05); the eye muscle area of ​​groups 2 and 3 increased by 9.4% (P <0.05) and 12.4% (P <0.01) respectively. The marbling score of the longissimus dorsi muscle in group 2 increased by 5.1% (P <0.05); the color score of the longissimus dorsi muscle in groups 3 and 4 increased by 13.6% and 8.1% respectively (P <0.01). Serum urea nitrogen and cholinesterase in the 2 groups decreased by 19.3% and 19.9% ​​respectively (P <0.05).

Application[2]

A method for treating crop straw is to combine calcium oxide, calcium hypochlorite, sodium bicarbonate, urea, calcium peroxide, sodium chloride, sodium glutamate, kelp powder, sodium p-aminophenylarsinate, The special treatment agent for quinol is dissolved in water. According to the ratio of treatment agent: straw powder: water = 1:80-120:100-270, mix thoroughly under stirring and put it into a container, compacting it while loading. Close the container and store at 4-36℃ for 72-180 hours. This method has simple process and low cost, effectively solves the problem of feed mildew, has a high crude fiber degradation rate, and the obtained feed is rich in nutrients and is easy to be absorbed by monogastric animals. It has opened up a method of monogastric animal feed using straw as raw material. important way.

Oxidation method[1]

Li Suqi et al. used LED light (λ=660 nm) as the excitation light source and methylene blue (MB) as the photosensitizer to generate singlet oxygen (1O2) to study the oxidative degradation of p-ASA in water by 1O2 to form inorganic arsenic. .At the same time, the effects of the initial pH of the system, light intensity, photosensitizer concentration and other factors on the reaction were investigated. The results showed that p-ASA was significantly degraded by the photosensitivity reaction and produced inorganic arsenic mainly As(V).p-ASA The degradation is significant under alkaline conditions; the degradation rate of p-ASA is positively correlated with the light intensity; the degradation rate of p-ASA first increases significantly with the increase of the concentration of photosensitizer MB, and tends to decrease after the concentration of MB exceeds 3 mg·L-1 Stable. Furfuryl alcohol (FFA) was selected as the reference substance, and the competitive kinetics method was used to estimate the reaction rate constant of 1O2 and p-ASA at pH=10 to be 7.44×106L·mol-1·s-1.

Main reference materials

[1]Li Suqi, Liu Zizheng, Wang Yunan, Li Jinjun, Wu Feng. Research on p-aminophenylarsonic acid oxidation in water with singlet oxygen [J]. Journal of Environmental Science, 2016, 36(08): 2852-2858.

[2] CN95104817.1 Crop straw treatment method and special treatment agent

[3] Tong Fudan, Xu Zirong. Effects of p-aminophenylarsonic acid combined with antibiotics on growth performance, carcass composition and blood biochemical indicators of hybrid pigs [J]. Chinese Journal of Animal Husbandry, 2001(06):24- 25.

[4] [1] Zhang Qian. Study on the toxic effects of nanop-aminophenylarsonic acid on SD rats [D]. Anhui Agricultural University, 2014.