Picryl Chloride

1.797 at 68 °F (NTP, 1992) - Denser than water; will sink

1.797 g/cu cm at 20 °C

Almost white needles

White needles or plates from chloroform, alcohol, & ligand

less than 1 mg/mL at 66 °F (NTP, 1992)

Freely sol in hot chloroform, benzene, boiling alcohol; slightly sol in ether or petroleum ether

Sol in ethanol; very sol in acetone

In water, 530 mg/L at 16 °C

181 to 185 °F (NTP, 1992)

83 °C

Picryl chloride appears as a detonating explosive in the form of light yellow needles. Slightly soluble in ether, alcohol, and benzene. Insoluble in water. As insensitive to shock as TNT. Primary hazard is blast of an instantaneous explosion, not flying projectiles or fragments. Under prolonged exposure to fire or heat the containers may explode violently.

Almost white solid; [Merck Index] White needle crystals; Wet with 20% water; [MSDSonline]

Danger

H201: (Deleted) Explosive; mass explosion hazard [Danger Explosives]

P210, P230, P240, P250, P260, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P320, P321, P330, P361+P364, P370+P380, P372, P373, P391, P401, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

H300+H310+H330 (100%): Fatal if swallowed, in contact with skin or if inhaled [Danger Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]

P260, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P320, P321, P330, P361+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Flash point data for this compound are not available, however, literature indicates that it is a flammable solid. (NTP, 1992)

· Flammable/combustible material.

SYMPTOMS: Exposure to this compound may cause irritation of the skin, respiratory tract or digestive tract. It may also cause dermatitis.

· Some are toxic and may be fatal if inhaled, ingested or absorbed through skin. Specifically, Dinitrophenol, wetted (UN1320); Dinitrophenolates, wetted (UN1321), Sodium dinitro-o-cresolate, wetted (UN1348); and Barium azide, wetted (UN1571) are known to be toxic.

Danger of skin sensitization; [MAK] Severe fire and explosion hazard; [Hawley] A potential sensitizer; [HSDB] A skin, digestive tract, and respiratory tract irritant; [CAMEO] Very toxic by inhalation, ingestion, and skin contact; [eChemPortal: ESIS] Explosive when dry; Toxic by ingestion, inhalation, or skin absorption; A severe eye irritant; [MSDSonline] See Picric acid.

/GUIDE 113: FLAMMABLE SOLIDS - TOXIC (WET/DESENSITIZED EXPLOSIVE)/ Fire or Explosion: Flammable/combustible material. May be ignited by heat, sparks or flames. DRIED OUT material may explode if exposed to heat, flame, friction or shock; treat as an explosive (GUIDE 112). Keep material wet with water or treat as an explosive (Guide 112). Runoff to sewer may create fire or explosion hazard. /Picryl chloride, wetted with not less than 10% water/

/GUIDE 113: FLAMMABLE SOLIDS - TOXIC (WET/DESENSITIZED EXPLOSIVE)/ Health: Some are toxic and may be fatal if inhaled, swallowed or absorbed through skin. Contact may cause burns to skin and eyes. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may cause pollution. /Picryl chloride, wetted with not less than 10% water/

/GUIDE 113: FLAMMABLE SOLIDS - TOXIC (WET/DESENSITIZED EXPLOSIVE)/ Public Safety: CALL Emergency Response Telephone Number. ... Isolate spill or leak area immediately for at least 100 meters (330 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Ventilate closed spaces before entering. /Picryl chloride, wetted with not less than 10% water/

/GUIDE 113: FLAMMABLE SOLIDS - TOXIC (WET/DESENSITIZED EXPLOSIVE)/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Structural firefighters' protective clothing will only provide limited protection. /Picryl chloride, wetted with not less than 10% water/

For more DOT Emergency Guidelines (Complete) data for 2-CHLORO-1,3,5-TRINITROBENZENE (8 total), please visit the HSDB record page.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

General First Aid:

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The following wastewater treatment technologies have been investigated for nitrobenzene: activated carbon. /Nitrobenzene/

The following wastewater treatment technologies have be investigated for nitrobenzene: biological treatment. /Nitrobenzene/

The following wastewater treatment technologies have been investigated for nitrobenzene: chemical precipitation. /Nitrobenzene/

For more Disposal Methods (Complete) data for 2-CHLORO-1,3,5-TRINITROBENZENE (6 total), please visit the HSDB record page.

Excerpt from ERG Guide 112 [Explosives - Division 1.1, 1.2, 1.3 or 1.5]:

Immediate precautionary measure

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

The effects of histamine, cimetidine, and diphenhydramine on picryl chloride (PCl)-induced ear contact sensitivity, as well as liver injury, were examined in mice. Histamine was found to produce less response in mice to PCl. In contrast, cimetidine, a selective antagonist of histamine type 2 receptor, significantly enhanced the response, while diphenhydramine, a selective antagonist of histamine type 1 receptor showed no effect. The pre-treatment of 2,4, 6-trinitrobenzene sulphonic acid (TNBS) significantly caused a tolerance to the formation of the liver injury induced by delayed-type hypersensitivity (DTH) to PCl. Against the tolerance, the single iv administration of 150 mg/kg cyclophosphamide (Cy) at 3 days before the TNBS-treatment recovered the response and induced a remarkable elevation of serum transaminases. On the other hand, cyclosporin A protected the liver injury. These observations revealed that the development of acute PCl-DTH liver injury was regulated by the functional state of suppressor and helper T cells.

... BALB/c mice were sensitized with 0.3% w/v 2,4,6-trinitro-1-chlorobenzene (TNCB) applied to the ear ... three times a week ... . Rolipram, prednisolone and cyclosporine A were administered orally once daily from day 0 to 21. Rolipram at a dose of 10 mg/kg/day significantly inhibited the ear thickness and the increase in cytokine levels and enzyme activity in the ear. Interleukin (IL)-4 production was markedly decreased in cervical lymph node cells from animals treated with rolipram at a dose of 10 mg/kg/day. Prednisolone and cyclosporine A significantly reduced ear thickness. These compounds significantly decreased the total cell and lymphocyte number of the cervical lymph nodes. Furthermore, prednisolone markedly suppressed body weight gain, and cyclosporine A significantly increased the serum total IgE concentration compared with that in the vehicle-treated control. Rolipram, unlike prednisolone and cyclosporine A, did not influence body weight and the total IgE concentration in the serum. The present results suggest that the PDE4 inhibitor is a promising oral medicine for the treatment of chronic skin inflammatory diseases.

... Oral administration of extract from Hatakeshimeji (Lyophyllum decastes, LD extract) to NC/Nga mice inhibited the development of atopic dermatitis-like skin lesions /induced by repeated application of picryl chloride/ based on lower total skin severity scores and serum immunoglobulin E (IgE) levels. Splenic lymphocytes were stimulated with the T cell mitogen concanavalin A, and secretion of a Th1 cytokine (IFN-gamma) and a Th2 cytokine (IL-4) was determined by ELISA. IFN-gamma production was not inhibited by treatment with LD extract. On the other hand, IL-4 production was significantly decreased by treatment with LD extract. These results suggest that LD extract exerts anti-allergic actions by suppressing the serum IgE and Th2-type immune responses.

... Rumex japonicus Houtt. (RJH) is one of the herbs used in Eastern countries for the treatment of atopic dermatitis (AD). It has been shown to have an antioxidative effect in human skin disease. ... To examine whether RJH extract (RJH-E) suppresses the development of AD-like skin lesions in NC/Nga mice, which are induced by the repeated application of picryl chloride (PC). ... symptom severity, scratching behavior, Staphylococcus aureus numbers on an ear, and serum levels of IgE, interleukin (IL)-4 and interferon (IFN)-gamma /were measured/. ... Oral administration of RJH-E to NC/Nga mice treated with PC inhibited the development of AD-like skin lesions as exemplified by a significant decrease in total skin symptom severity scores, and a decrease in hypertrophy, hyperkeratosis and infiltration of inflammatory cells in the skin. The scratching behavior and numbers of S. aureus, which are known to be exacerbated in AD, were also significantly reduced by RJH-E. No significant change was observed in the serum levels of IFN-gamma, whereas IgE and IL-4 levels were significantly reduced by RJH-E. ...

For more Interactions (Complete) data for 2-CHLORO-1,3,5-TRINITROBENZENE (16 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 140(SRC), determined from a water solubility of 530 mg/L at 16 °C(2) and a regression-derived equation(3), indicates that 2-chloro-1,3,5-trinitrobenzene is expected to have high mobility in soil(SRC). Volatilization of 2-chloro-1,3,5-trinitrobenzene from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.5X10-10 atm-cu m/mole(SRC), using a fragment constant estimation method(4). 2-Chloro-1,3,5-trinitrobenzene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.1X10-5 mm Hg(SRC), determined from a fragment constant method(5). 2-Chloro-1,3,5-trinitrobenzene is expected to be resistant to biodegradation under aerobic conditions in soil(SRC) as the presence of multiple nitro groups and a halogen group, as found in its structure, have been reported to decrease biodegradability(6). 2-Chloro-1,3,5-trinitrobenzene is expected to slowly hydrolyze in water with a half-life of 127 days at pH 7(7).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 140(SRC), determined from a water solubility of 530 mg/L at 16 °C(2) and a regression-derived equation(3), indicates that 2-chloro-1,3,5-trinitrobenzene is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.5X10-10 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 18(SRC), from its water solubility (2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). 2-Chloro-1,3,5-trinitrobenzene is expected to be resistant to biodegradation under aerobic conditions in water(SRC) as the presence of multiple nitro groups and a halogen group, as found in its structure, have been reported to decrease biodegradability(6). 2-Chloro-1,3,5-trinitrobenzene is expected to slowly hydrolyze in water with a half-life of 127 days at pH 7(7).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2-chloro-1,3,5-trinitrobenzene, which has an estimated vapor pressure of 1.1X10-5 mm Hg at 25 °C (SRC), determined from a fragment constant method(2), is expected to exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase 2-chloro-1,3,5-trinitrobenzene is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 42,000 days(SRC), calculated from its rate constant of 3.8X10-16 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase 2-chloro-1,3,5-trinitrobenzene may be removed from the air by wet or dry deposition(SRC). 2-Chloro-1,3,5-trinitrobenzene contains chromophores that absorb at wavelengths >290 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC).

The Koc of 2-chloro-1,3,5-trinitrobenzene is estimated as 140(SRC), using a water solubility of 530 mg/L at 16 °C(1)and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that 2-chloro-1,3,5-trinitrobenzene is expected to have high mobility in soil.

2-Chloro-1,3,5-trinitrobenzene's former production and use in acrylate adhesives, epoxy resin, as a polyisocyanate mixture stabilizer, and in concrete and gypsum impregnation (1) and its current use as a research chemical(2) may result in its release to the environment through various waste streams(SRC).

AEROBIC: 2-Chloro-1,3,5-trinitrobenzene is expected to be resistant to biodegradation under aerobic conditions(SRC) as the presence of multiple nitro groups and a halogen group, as found in its structure, have been reported to decrease biodegradability(1).

An estimated BCF of 18 was calculated for 2-chloro-1,3,5-trinitrobenzene(SRC), using a water solubility of 530 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for 2-chloro-1,3,5-trinitrobenzene is estimated as 2.5X10-10 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 2-chloro-1,3,5-trinitrobenzene is expected to be essentially nonvolatile from water surfaces(2). 2-Chloro-1,3,5-trinitrobenzene's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). 2-Chloro-1,3,5-trinitrobenzene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.1X10-5 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... This study ... first investigated the cellular immune responses in mice with chronic liver injury induced by delayed-type hypersensitivity to picryl chloride (PCl). A continuous reduction, after week 3 of liver injury, was observed in the level of PCl-induced contact sensitivity but not in sheep red blood cell-induced footpad reaction, suggesting the presence of PCl-specific suppression. When spleen cells from mice whose liver had been injured for 1 week were systemically transferred into syngeneic recipients with the liver injury, the elevation in serum lactic dehydrogenase and the decrease in alkaline phosphatase and albumin levels in recipient mice were significantly exacerbated. However, when the liver damage in the donor mouse was allowed to proceed for 3, 5 or 7 weeks, biochemical changes in recipients were reduced to near normal levels. A flow-cytometric assay demonstrated that the number of CD4+ T cells in both spleen cells and liver nonparenchymal cells decreased dramatically during the late phase of liver injury, while CD8+ counts did not. These findings suggest that CD4+ and CD8+ T lymphocytes may contribute to the positive and negative regulation, respectively, of the early and late phases in the chronic development of liver injury.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The developmental characteristics of liver injury induced by a delayed-type hypersensitivity (DTH) mechanism against picryl chloride were examined for 9 consecutive weeks in 3 mouse strains, BALB/c, Kunming and ICR mice. The changes of most biochemical parameters were similar in these three strains, namely, the activities of serum transaminases, lactic dehydrogenase, and prolidase were elevated significantly on day 1, during the first several weeks, and almost throughout the duration, respectively, of liver injury. The content of liver hydroxyproline was also increased after 1-9 weeks of liver injury. In addition, a significant decrease of liver weight, serum alkaline phosphatase and albumin level was observed in BALB/c and Kunming mice. Similar changes in liver histology were also found in the three strains. The hepatocellular necrosis and inflammatory infiltration into the portal area were the predominant features on day 1 and were still distinct during the subsequent several weeks. The mild or moderate hepatocellular degeneration, regeneration and connective tissue hyperplasia were observed after 1 or 3 weeks. A bridging necrosis between portal and portal was observed in several BALB/c and ICR mice, reflecting the possibility of exacerbation of liver injury. ...

/IMMUNOTOXICITY/ Lymph node cells from BALB/k mice, but not from BALB/c mice, immunized with picryl chloride (PCl) produce IL-5 when stimulated with the specific antigen in vitro and this correlates with picryl-specific IgA levels in vivo, which are 6 to 10 times higher in BALB/k mice. B lymphocytes from BALB/k mice cultured with PCl-immune T cells from BALB/k produce in vivo anti-PCl-IgA, while B lymphocytes from BALB/c mice, cultured with T cells from BALB/c mice, fail to produce appreciable amounts of anti-PCl IgA, unless IL-5 is added to cultures. ...

/IMMUNOTOXICITY/ Ear skin responses to picryl chloride (PCL)-induced contact dermatitis were compared in detail between IQI/Jic mice developed in Japan and BALB/c mice often used for the investigation of contact dermatitis. PCL was applied to the left ear of each mouse 4 (1st), 11 (2nd), 18 (3rd) and 25 days (4th) after sensitization of the abdominal skin with PCL. Time course examinations were carried out on the ear swelling responses, total IgE levels, skin histology and immunohistochemistry for infiltrated cells after the 1st and 4th application. In IQI mice, the peak time of the ear swelling responses tended to shift from 24 hr to 9 hr with marked elevation of total IgE levels and marked increase of mast cells showing degranulation after the 4th application when CD8(+) cells as well as CD4(+) cells also prominently increased. In BALB/c mice, except for the total IgE levels and the number of mast cells, the degrees of ear swelling responses, histological changes and increase of CD4(+) and CD8(+) cells were much less severe. Female IQI mice are considered to be a useful mouse strain for further investigations on the role of CD4(+) and CD8(+) T cells in the pathogenesis of contact dermatitis.

For more Non-Human Toxicity Excerpts (Complete) data for 2-CHLORO-1,3,5-TRINITROBENZENE (13 total), please visit the HSDB record page.

The rate constant for the vapor-phase reaction of 2-chloro-1,3,5-trinitrobenzene with photochemically-produced hydroxyl radicals has been estimated as 3.8x10-16 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 42,000 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 2-Chloro-1,3,5-trinitrobenzene contains chromophores that absorb at wavelengths >290 nm(2) and therefore may be susceptible to direct photolysis by sunlight(SRC). A hydrolysis rate constant of 6.44x10-8 L/mole-sec(SRC) was measured for 2-chloro-1,3,5-trinitrobenzene at pH 7, corresponding to a half-life of 127 days(3).

Occupational exposure to 2-chloro-1,3,5-trinitrobenzene may have occurred during its former production through inhalation of dust and dermal contact with this compound at workplaces where 2-chloro-1,3,5-trinitrobenzene was produced or used. (SRC)

Trinitrochlorobenzene

A Commercial Grade

5000

A Commercial Grade

400

Explosive chemical that can be released at a facility.

It has been predicted that a type-1 and type-2 helper T cell (Th1/Th2) imbalance exists in atopic dermatitis (AD). In DS-Nh mice, an AD mouse model, Staphylococcus aureus increases on the skin surface. ... To investigate whether the Th1-dominant response has an influence on the development of AD, ... chronic allergic hypersensitivity with 2,4,6-trinitrochlorobenzene (TNCB ) /was induced/ in two AD mouse models: NC/Nga mice and DS-Nh mice. Th1 and Th2 cytokine production of splenocytes was assessed under stimulation with staphylococcal enterotoxin B (SEB) which induces a Th1 response in DS-Nh mice with or without TNCB sensitization. ... Clinical skin changes, transepidermal water loss (TEWL), the number of S. aureus on the skin and the serum IgE levels /was examined/ in these mice treated repeatedly with TNCB under conventional conditions (free of fur mites). The splenocytes of DS-Nh mice were cultured with SEB and the cytokine levels in the supernatants were measured by enzyme-linked immunosorbent assay (ELISA). ... Significant skin changes were observed on the skin even where TNCB was not applied in both mice treated with TNCB. Increases in S. aureus on the skin and serum IgE levels were detected in DS-Nh mice, but not in NC/Nga mice. In DS-Nh mice, IFN-gamma and IL-13 production of splenocytes increased in the mice treated with TNCB. /THe authors concluded that/ these results suggest that there might be a different mechanism of dermatitis induction between NC/Nga and DS-Nh mice. Th1 responses might play an important role in the development of dermatitis and increase in serum IgE levels in DS-Nh mice through an increase in IL-13 production.

... A new model of liver injury induced in mice by delayed-type hypersensitivity (DTH) to picryl chloride (PCl) mimicks the pathogenesis of human hepatitis /was reported/. This liver injury is mediated by CD4+ T cells. The interaction between lymphocyte function associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1) is an essential process for hepatocyte (HC) damage. The present study was undertaken to reveal the role of Th1 and Th2-like cytokines in regulating the liver injury. ... The kinetics of cytokine production were examined by ELISA and RT-PCR after the elicitation of liver injury for both serum protein and liver mRNA expression, respectively. A co-culture assay between liver nonparenchymal cells (NPC) and HC was conducted to evaluate the cytokine regulation on the cell-cell interaction. Expression of LFA-1 on NPC and ICAM-1 on HC were examined by FACScan and ELISA, respectively. ... Serum IL-2 and IFN-gamma showed a peak production at 6 and 12 hr, while IL-5 and IL-4 reached their maximum levels at 18 and 24 hr after induction of liver injury, respectively. Liver mRNA expression of IFN-gamma and IL-4 had a similar time course to their corresponding products. Both recombinant murine IFN-gamma and IL-2 triggered the hepatotoxicity of NPC or spleen cells at 0 h. In this case, an increased expression of both LFA-1 on NPC and ICAM-1 on HC was also observed. In contrast, IL-4 and IL-5 completely abolished the hepatotoxicity of NPC at 12 hr without influencing the adhesion molecules. /The authors concluded that/ Th1 and Th2 may be involved in regulating liver injury. Th1/Th2 balance may critically contribute to the production of the liver injury or recovery from it.

The kinetics of lymphocyte function associated antigen 1 (LFA-1) expression on spleen cells (SPC) and liver non-parenchymal cells (NPC), and intercellular adhesion molecule 1 (ICAM-1) expression on hepatocytes (HC) was examined in acute liver injury mice induced by a DTH reaction to picryl chloride (PCl). The peak expression of LFA-1 on SPC was seen at 6 hr after eliciting liver injury, and then that of LFA-1 on NPC and ICAM-1 on HC appeared at 12 hr. Thereafter, the serum ALT elevation reached to a peak at 18 hr. A splenectomy before the PCl elicitation significantly reduced the ALT elevation. Both SPC and NPC from liver injury mice induced a remarkable release of ALT from HC in vitro, in parallel with their LFA-1 expression. The pre-treatment of NPC or SPC with anti-LFA-1 mAb, irrespective of the presence of complement, completely blocked the ALT release. Also, when HC was prebound with anti-ICAM-1 mAb, neither NPC nor SPC showed a cytotoxicity against the HC. Furthermore, the treatment of NPC with either anti-Thy1.2 or anti-CD4 mAb in the presence but not absence of complement, showed a complete abolishment of ALT release. Anti-CD8 mAb plus complement also tended to inhibit ALT release. The twofold increase in CD4+ LFA-1+ and mild increase in CD8+ LFA-1+ populations were also confirmed in NPC at 12 hr. These results suggest that PCl elicitation in liver may trigger an increased expression of LFA-1 on SPC and NPC and ICAM-1 on HC. LFA-1/ICAM-1 interaction between liver-infiltrating NPC, mainly including CD4+ and CD8+ T cells, and HC may be an essential step for the hepatocyte damage in PCl-DTH liver injury.

Liver injury was induced in BALB/c mice by local delayed-type hypersensitivity (DTH) to picryl chloride (PC1). Distinct changes of biochemical parameters were observed including the elevation of serum alanine and aspartate aminotransferases, increase of liver lipid peroxides, as well as decrease of serum alkaline phosphatase. Damage was confirmed by histopathological findings such as hepatocellular necrosis, granulocyte infiltration, and fatty degeneration. The liver injury was passively transferred into naive syngeneic mice by infusing spleen cells from immune mice. The capacity of the splenocytes to induce liver injury in recipient mice was almost completely abolished by pretreatment of the cells with anti-Thy 1.2 or anti-CD4, but not anti-CD8 antibody. These findings suggest that the production of liver injury by a local DTH mechanism is possible and the subpopulation of T cells, Thy-1.2+, L3T4+, and Lyt-2- cells, is at least one of the effector cells that mediate the injury.

For more Mechanism of Action (Complete) data for 2-CHLORO-1,3,5-TRINITROBENZENE (10 total), please visit the HSDB record page.

The fate of (14)C-picryl chloride (PCl) injected intradermally into ears of guinea pigs at minimal sensitizing dose 0.25 ug was followed during induction period of delayed hypersensitivity. Approx 50% PCl rapidly escaped from ear in 3 hr; decomposition products were in urine within 3-4 hr.

Used in acrylate adhesives and epoxy resins; Also used in polyisocyanate mixture stabilization and concrete and gypsum impregnation; [HSDB]

Working with Glues and Adhesives [Category: Other]

Known uses: acrylate adhesives, epoxy resin, polyisocyanate mixture stabilizer, concrete and gypsum impregnation