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Biomedical subjects

G F Gerberick

Publications and source records attributed to G F Gerberick.

At least 55 records · Page 3Linked to original sources
PubMed1996

An interlaboratory evaluation of the Buehler test for the identification and classification of skin sensitizers.

The correct identification of potential skin sensitizers is an essential first step in enabling a proper risk assessment to be made and to permit the implementation of appropriate risk management practices designed to avoid the induction of sensitization. Consequently, regulatory guidelines around the world demand that new substances are evaluated to assess their skin sensitization potential. There are two guinea pig test methods which are generally recognised, the guinea pig maximisation test (GPMT) and the occluded patch test described by Buehler. In different countries, one procedure seems to be more prevalent and acceptable to regulatory authorities than the other. Notably, in the European Union, the latest revision of the Annex V (Directive 92/32/EC) Test Method for skin sensitization asks that justification should be given in the situation where the notifier does not use the GPMT, which is the preferred method. Thus in this paper, the validity of the Buehler protocol in the context of European legislation is critically examined. Results from two laboratories are collated, showing that the method can identify significant contact allergens, particularly those which would be registered formally as such according to European legislation. It is demonstrated that minor methodological variations can be tolerated without compromising test sensitivity, but it is recommended that suitable positive control testing is the best way to ensure proper test conduct.

1-Propanol↗
PubMed1995

An international evaluation of the murine local lymph node assay and comparison of modified procedures.

The murine local lymph node assay is a predictive test for the identification of skin-sensitizing chemicals. The method has been the subject both of national inter-laboratory studies and of extensive comparisons with guinea pig tests. In the investigations reported here, the local lymph node assay has been evaluated further in the context of an international study comprising five independent laboratories. In addition, the influence of minor modifications to the standard assay procedure on the performance of the test has been examined. The modified procedures investigated were exposure of mice for 4 rather than 3 consecutive days, excision of lymph nodes 4 rather than 5 days after the initiation of exposure and the use of an alternative isotope. All five laboratories, irrespective of whether the standard or a modified protocol was used, were able to identify accurately, and with comparable sensitivity, potassium dichromate and 2,4-dinitrochlorobenzene as skin sensitizers. Using standard criteria, none of the laboratories recorded positive responses with methyl salicylate, a non-sensitizer. In the standard protocol, lymph nodes are pooled for each experimental group and the vigor of responses measured as a stimulation index relative to vehicle controls. A stimulation index of 3 or greater is considered to indicate skin-sensitizing potential. One further modification adopted by three of the laboratories was to analyze nodes from individual animals and, thereby, permit statistical evaluation. This allowed a direct comparison of statistical significance with the conventional stimulation index as criteria for a positive response. The data indicate that, while statistical evaluation may provide, in some instances, for small increases in sensitivity, this may be at the expense of some loss of selectivity. There are, however, insufficient data presently to draw firm conclusions regarding the relative value of statistical analysis. These studies demonstrate that the local lymph node assay is sufficiently robust to accommodate minor procedural and technical modifications without material changes in test performance.

Analysis of Variance↗
PubMed1995

Cumulative effects from repeated exposures to suberythemal doses of UVB and UVA in human skin.

BACKGROUND: The skin is repeatedly exposed to solar UV radiation. Long-term photodamage is a consequence of cumulative UV radiation injury. Hence an examination of the repetitive effects of UV exposure is more likely to yield clues to the early alterations that lead to photoaged skin than a single exposure. OBJECTIVE: We examined the effects of repetitive low-dose UV irradiation on human skin with the aim of identifying UVA-induced effects that may have a different wavelength dependence than acute erythema. METHODS: Areas on the lower part of the back were each exposed to a suberythemal dose (0.5 minimal erythema dose [MED]) of solar simulated radiation (290 to 400 nm) and of UVA (320 to 400 nm) once daily, 5 days a week, for 28 doses. One site was also treated daily with a sunscreen having a sun protection factor of 22 and then exposed to 11 MEDs of solar simulated radiation for the same duration. Epidermal and dermal changes were analyzed and quantified by histochemical stains in combination with computer-assisted image analysis of tissue sections. RESULTS: At equal 0.5 MED doses, UVA induced greater cumulative changes than solar simulated radiation, as assessed by development of a greater cumulative erythema response in the first week of treatment, the presence of epidermal hyperplasia and stratum corneum thickening, depletion of Langerhans cells, dermal inflammatory infiltrates, and deposition of lysozyme on elastin fibers. These changes were not prevented by the sunscreen. A single short-term dose of UVA did not elicit these changes. CONCLUSION: These findings suggest that UVA may contribute significantly to long-term actinic damage and that the spectral dependence for cumulative damage does not parallel the action spectrum for acute injury (erythema) in human beings.

Adult↗
PubMed1994

Risk assessment of sensitizing agents.

This review describes an approach that has been used to assess the skin sensitization risk of new product ingredients prior to and after marketing. The risk assessment process utilizes a comparative toxicological approach in which data on the inherent toxicity of a material and the exposure to it through manufacturing or consumer use or foreseeable misuse are integrated and compared with data generated by 'benchmark' materials of similar chemistry or product application, or both. This approach has been valuable in providing an accurate assessment of skin sensitization potential and the basis for eventual safe marketing of a wide range of consumer household and personal care products and topical pharmaceuticals.

Animals↗
PubMed1994

Increases in human epidermal DR+CD1+, DR+CD1-CD36+, and DR-CD3+ cells in allergic versus irritant patch test responses.

In an attempt to differentiate an allergic patch test response from an irritant response, we evaluated by flow cytometry the percentages of various epidermal cell populations isolated from allergen and irritant-treated patch test sites. Nine allergic individuals were patch tested with various allergens (Rhus, dinitrochlorobenzene [DNCB], or nickel chloride) and a vehicle control for 48 h. Eight additional individuals were patch tested with irritating chemicals (sodium lauryl sulfate or nonanoic acid) and with a vehicle control for 48 h. Epidermal cells, isolated from suction blisters, were double labeled for CD1/HLA-DR, CD3/HLA-DR, or CD36/HLA-DR cell surface markers and analyzed by flow cytometry to determine the percentage of various cell populations. A mean increase of 0.91 +/- 0.3 in the percentage of DR+CD1+ Langerhans cells over the vehicle control patch test site was detected in allergen-positive patch test sites in allergic individuals, whereas a decrease of 0.19 +/- 0.2 in the percentage of DR+CD1+ Langerhans cells from the vehicle control patch test site was detected in irritant-treated patch test sites. Epidermal cells from allergen-positive patch test sites also exhibited an increase of 5.2 +/- 1.8 in percentage of DR+CD1- cells over the vehicle control patch test site compared to an increase change of 0.8 +/- 0.4 in epidermal cells isolated from irritant-treated patch test sites. We also found that DR+ cells that lacked the CD1 determinant expressed the macrophage/monocyte antigen CD36 (OKM5). Finally, a 2.3 +/- 0.8 increase in the percentage of DR-CD3+ cells over the vehicle control patch test site was observed in allergen-positive patch test sites compared to an increase of 0.2 +/- 0.2 observed in irritant-treated patch test sites. These results demonstrate a significant increase in DR+CD1+, DR+CD1-CD36+, and DR-CD3+ epidermal cells in allergen-positive patch test sites compared to irritant patch test sites.

Adult↗
PubMed1992

Chemical allergy: molecular mechanisms and practical applications.

Allergic reactions can be defined as the adverse, tissue-damaging, and sometimes fatal consequences of specific immune responses, usually to exogenous antigens. In the context of toxicology it is allergic reactions resulting from immune responses to chemicals and drugs which are of greatest relevance. The allergy may take a variety of forms including contact hypersensitivity (allergic contact dermatitis), respiratory hypersensitivity (with symptoms ranging from mild rhinitis to severe asthma), and various types of comparatively ill-defined reactions which in many respects resemble autoimmunity. Of these contact hypersensitivity is the most frequently encountered health problem resulting from the interaction of chemicals with the immune system. A wide variety of chemicals are able to induce contact sensitization. Some of these are, in addition, known to cause respiratory hypersensitivity, a less frequent, but no less important, form of chemical allergy.

Animals↗
PubMed1992

Examination of the local lymph node assay for use in contact sensitization risk assessment.

The purpose of this study was to evaluate the utility of the murine local lymph node assay (LLNA) for contact sensitization risk assessment. Cellular proliferative activity in draining lymph nodes was determined for individual animals on Day 5 following four daily epicutaneous applications of the test chemical to the ears. Seventeen chemicals were tested, covering a range of materials including preservatives, drug actives, and perfume raw materials. The assay was found to be useful for identifying strong, moderate, and some weak sensitizers as defined by other testing methods (guinea pig, human). For evaluating the antigen specificity of the LLNA proliferative response, an in vitro blastogenesis assay was used. Dendritic cells (DC) isolated from lymph nodes of mice treated 24 hr earlier with trinitrochlorobenzene (TNCB) were capable of in vitro stimulation of lymphocytes from TNCB-sensitized mice, but not lymphocytes from mice sensitized to the preservative mixture of 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone (MCI/MI). Conversely, DC from mice treated 24 hr earlier with MCI/MI were capable of stimulating lymphocytes from MCI/MI-sensitized mice, but were unable to stimulate lymphocytes from TNCB-sensitized mice, demonstrating the specificity of the response. The results of these studies support the use of the murine LLNA for both investigative and predictive contact sensitization testing. The LLNA offers the advantages of requiring less time for completion, incorporating an objective endpoint, requiring approximately half the number of animals, and being less costly than most currently employed guinea pig test methods. In addition, we believe the murine LLNA is a useful test to incorporate into a scheme for contact sensitization risk assessment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Examination of tetrachlorosalicylanilide (TCSA) photoallergy using in vitro photohapten-modified Langerhans cell-enriched epidermal cells.

Lymphocytes from BALB/c mice photosensitized in vivo to tetrachlorosalicylanilide (TCSA) were investigated to determine whether they could be stimulated to proliferate when cultured with Langerhans cell-enriched cultured epidermal cells (LC-EC) photohapten-modified in vitro with TCSA + UVA radiation. Cultured LC-EC were photohapten-modified in vitro by irradiation in TCSA-containing medium using a 1000-watt solar simulator equipped with filters to deliver primarily UVA radiation (320-400 nm). Lymphocytes from TCSA-photosensitized mice were incubated with LC-EC that had been treated in vitro with 0.1 mM TCSA and 2 J/cm2 UVA radiation (TCSA + UVA). Responder lymphocytes demonstrated a significant increase in their blastogenesis response compared to lymphocytes that were incubated with LC-EC irradiated with UVA prior to treatment with TCSA (UVA/TCSA) or with LC-EC that had received no treatment. Lymphocytes from naive mice or mice photosensitized with musk ambrette (MA) demonstrated a significantly lower response to LC-EC modified with TCSA + UVA, indicating the specificity of the response. Maximum blastogenesis response was achieved when LC-EC were treated with 0.1 mM TCSA and a UVA radiation dose of at least 0.5 J/cm2. Epidermal cells depleted of LC by treatment with anti-Ia antibody plus complement or by an adherence procedure were unable to stimulate this blastogenesis response. Epidermal cells treated in vitro with TCSA + UVA demonstrated enhanced fluorescence compared to control cells. The fluorescence observed was not restricted to any specific epidermal cell type; however, fluorescence microscopy studies revealed that dendritic Ia-positive cells, presumably LC, were also TCSA fluorescent. Flow cytometry showed that Ia-positive epidermal cells demonstrated the greatest UV fluorescence when treated with TCSA + UVA compared to both cells irradiated with UVA and subsequently treated with TCSA and untreated cells. This is consistent with the enhanced antigen presentation capability of TCSA + UVA treated LC-EC, which leads to the conclusion that LC photohapten-modified in vitro with TCSA + UVA demonstrate enhanced TCSA fluorescence and are capable of stimulating lymphocytes from TCSA photosensitized mice in an antigen-specific manner.

Animals↗
PubMed1991

Increased number of dendritic cells in draining lymph nodes accompanies the generation of contact photosensitivity.

Draining lymph node cells isolated from mice 48 h after topical exposure to tetrachlorosalicylanilide (TCSA) + UVA radiation (TCSA + UVA) demonstrated a two-fivefold increase in the number of dendritic cells (DC) compared with control mice treated with vehicle + UVA. The increase in number of DC was both time and dose dependent, with the peak DC accumulation occurring at 48 h post application and at a TCSA dose of 1.0%. Photospecificity was evident in that mice irradiated prior to treatment with TCSA (UVA/TCSA) demonstrated no significant increase in DC accumulation. The accumulation of DC was followed by a significant increase in total lymph node cellularity. An in situ 3H-thymidine incorporation assay showed a significant increase in proliferative activity of cells isolated from the draining lymph nodes of mice treated with TCSA + UVA as compared to naive, vehicle, or UVA/TCSA-treated mice. Dendritic cells isolated from mice treated 24 h earlier with TCSA + UVA, but not those from naive mice or mice treated with UVA/TCSA, were capable of TCSA-specific antigen presentation. Responder lymphocytes from untreated mice or mice photosensitized with musk ambrette showed a much lower response to DC isolated from TCSA + UVA-treated mice, demonstrating the specificity of the reaction. DC-depleted lymph node cells were unable to stimulate this blastogenesis response. These results suggest that application and photoactivation of TCSA induces cellular and functional changes in the lymph node DC indicative of their involvement in the induction phase of a contact photoallergic reaction.

Allergens↗
PubMed1990

A predictive mouse ear-swelling model for investigating topical photoallergy.

The photoallergic potential of various compounds was assessed using a mouse ear-swelling model, which offers the advantage of being quantifiable and more objective than models based on subjective evaluation of erythematous skin reactions. Cyclophosphamide pretreated BALB/c mice were induced by topical treatment of the dorsal skin surface on 3 consecutive days and challenged on the ears 5 days after the last induction. For each induction and challenge treatment, mice were consecutively irradiated with ultraviolet (UV) A (10 J/cm2) and UVB (45 mJ/cm2) radiation 30 min to 1 hr after test material application. The photoallergic response to musk ambrette, a known human photoallergen, was significantly augmented when three consecutive induction exposures were used as compared with one or two inductions. The photoallergic potential of nine other known human photoallergens (tetrachlorosalicylanilide, bithionol, 6-methylcoumarin, chlorpromazine, sodium omadine, bisphenol A, sulphanilamide, fentichlor and p-aminobenzoic acid) was successfully detected using the mouse model. In each experiment, the ear thickness changes observed in the photoallergy test mice were significantly greater than the changes observed in the contact allergy, vehicle/radiation and phototoxicity control mice. Coumarin and homosalate, two agents not traditionally associated with causing photoallergy in humans or animals, did not demonstrate contact photoallergy using this model. With three of the photoallergens, musk ambrette, bithionol and tetrachlorosalicylanilide, the ear swelling response obtained was due to photoallergy alone and not due to the co-existence of both contact photoallergy and contact allergy. In addition, irradiating mice 24 hr, rather than 1 hr, following application of the test material during the induction phase resulted in a significantly reduced photoallergic response with both musk ambrette and tetrachlorosalicylanilide. These results indicate that the mouse ear-swelling model is a potentially useful model for investigative and predictive photoallergy testing.

Administration, Topical↗
PubMed1990

Use of UVB and UVA to induce and elicit contact photoallergy in the mouse.

The development of a contact photoallergic response in animals or humans requires irradiation of the test material. Since consumers are exposed to both UVB and UVA radiation following the use of topically applied products, we have developed a mouse ear swelling photoallergy model for the screening of potential photoallergens. This model incorporates the use of UVB, as well as UVA, radiation for the induction and elicitation phases of the photoallergic response. In this report, we show that the use of a 10 J/cm2 UVA and 45 mJ/cm2 UVB dose regimen during both the induction and elicitation phases results in an augmented photoallergic response to 6-methylcoumarin as compared with the responses of mice treated with 6-methylcoumarin and irradiated with UVA or UVB alone or UVA plus UVB radiation for induction and then UVA or UVB radiation alone at challenge. Photoallergic responses to tetrachlorosalicylanilide and musk ambrette were neither augmented nor diminished by the use of UVB radiation at induction and challenge as compared with the use of UVA treatment alone. The non-photocontact allergic response to oxazolone was reduced approximately 25% when mice were treated with oxazolone plus UVB and UVA radiation as compared with mice treated with oxazolone alone. These results suggest that in screening a test material's photoallergic potential, UVB and UVA radiation should be included for both the induction and elicitation phases of the mouse ear swelling photoallergy protocol.

Allergens↗
PubMed1989

A predictive mouse ear-swelling model for investigating topical phototoxicity.

Predictive models should be used to determine the phototoxic potential of consumer products intended for topical exposure and outdoor use. To determine the potential of a compound to elicit a phototoxic reaction, a mouse ear-swelling model, which uses a xenon arc ultraviolet (UV) solar simulator as the radiation source, was used. The UV solar simulator delivered UV radiation from 290 to 400 nm (UVB + UVA) or from 320 to 400 nm (UVA) when appropriate filters were used. With this model, the phototoxic potential of nine known phototoxins and three negative test materials was successfully demonstrated. Based on the time of onset of the phototoxic response following test material application and irradiation, both immediate (20-30 min) and delayed-type (48-96 hr) phototoxic responses were demonstrated using this model with anthracene and 8-methoxypsoralen, respectively. The optimal time for irradiation after application of 8-methoxypsoralen to the ears was 30-60 min. Irradiation of ears immediately after treatment with 8-methoxypsoralen or 6 hr after application resulted in little or no phototoxic response. The phototoxic response to 8-methoxypsoralen was dependent upon the UVA dose and, when tested at a constant UVA dose, the response was concentration dependent. To obtain an optimal phototoxic response to 7-methoxycoumarin, both UVB and UVA radiation were required. These results show that the mouse ear-swelling model, which is quantifiable and more objective than models based on subjective evaluation of skin changes, is an excellent model for investigative and predictive phototoxicity testing.

Administration, Cutaneous↗
PubMed1989

Contact photoallergy testing of sunscreens in guinea pigs.

The potential of 3 sunscreens (p-aminobenzoic acid, 4-isopropyldibenzoylmethane and homosalate) and 2 known human photoallergens (musk ambrette and tetrachlorosalicylanilide) to cause photoallergy, phototoxicity, and/or contact sensitization was determined using a guinea pig photoallergy model, as previously described by Harber and associates. The model was slightly modified by employing 6 exposures over 2 weeks and using Hill Top Chambers for application of the test material. Contact photoallergy was detected in guinea pigs treated with musk ambrette or tetrachlorosalicylanilide (TCSA), although with TCSA, a lower incidence of contact sensitivity and phototoxicity was also detected. The results of studies conducted with sunscreens showed that p-aminobenzoic acid was photoallergenic, whereas homosalate and 4-isopropyl-dibenzoylmethane (Eusolex 8020) were not. However, contact sensitization, and to a lesser degree primary irritation, was detected with Eusolex 8020 at the concentrations employed in this study. The results of these studies suggest that this guinea pig model is a suitable model for assessing the photoallergic potential of various compounds, including the sunscreens tested in this study.

4-Aminobenzoic Acid↗
PubMed1986

Relationships between pulmonary inflammation, plasma transudation, and oxygen metabolite secretion by alveolar macrophages.

We have previously shown that alveolar macrophages from normal rabbit lungs do not synthesize reactive oxygen intermediates unless first conditioned by culture in vitro in the presence of serum for 24 to 48 hr. This conditioning process is mediated by a serum constituent that partitions on gel exclusion columns with an apparent m.w. of 30,000 to 50,000 daltons. Alveolar macrophage conditioning in vitro requires protein synthesis, is associated with the generation of membrane NADPH oxidase activity, and is reversible. We have predicted therefore that during the course of pulmonary inflammation, as observed 3 wk after i.v. injection of M. butyricum in oil, alveolar macrophages might similarly become conditioned in vivo through exposure to plasma protein transudates reaching the alveolus. In support of this hypothesis we show that after experimental production of granulomatous pulmonary inflammation in rabbits, alveolar macrophages showed an augmented capacity to secrete superoxide anion when stimulated with phorbol ester, and this enhancement increases exponentially with increased plasma transudation. This augmented enhancement was reversible, and decreased after culture in vitro in the absence of serum. Mature alveolar macrophages were responsible for this enhanced superoxide anion production rather than freshly emigrated monocytes. Moreover, superoxide anion production in this model of pulmonary inflammation appears to be an "all-or-none" phenomenon, with superoxide anion production associated with a subpopulation of optimally conditioned alveolar macrophages, whereas the remaining unconditioned alveolar macrophages produce little or none. We feel that these two classes of alveolar macrophages may be derived from inflamed and noninflamed regions of the lung, respectively, thereby reflecting the discontinuous nature of the inflammatory lesions themselves. Thus we propose that measurements of reactive oxygen intermediate production by lavaged alveolar macrophages may provide a semi-quantitative measure of chronic pulmonary inflammation.

Animals↗
PubMed1986

Toxicity of mycotoxins for the rat pulmonary macrophage in vitro.

The presence of mycotoxins in grains is well documented. Workers in grain handling occupations are commonly exposed to grain dust aerosols. Work in our laboratory has shown that T-2 toxin is highly toxic to rat alveolar macrophages in vitro, causing loss of viability, release of radiolabeled chromium, inhibition of macromolecular synthesis, inhibition of phagocytosis, and inhibition of macrophage activation. Similarly, patulin caused a significant release of radiolabeled chromium, decrease in ATP levels, significant inhibition of protein and RNA synthesis, and inhibition of phagocytosis. The data show that both T-2 toxin and patulin are highly toxic to rat alveolar macrophages in vitro. The data further suggest that the presence of these mycotoxins in airborne respirable dust might present a hazard to exposed workers.

Animals↗
PubMed1985

Serum factor requirement for reactive oxygen intermediate release by rabbit alveolar macrophages.

Alveolar macrophages (AM) from pathogen-free rabbits were unable to release reactive oxygen intermediates (ROI) unless they were conditioned in serum for 24-48 h before triggering with membrane-active agents. The degree of serum conditioning of AM depended upon the concentration of serum used; optimal ROI release was obtained at or above 7.5% fetal bovine serum (FBS). FBS, autologous rabbit serum, pooled rabbit serum, and pooled human serum were each capable of conditioning AM for release of ROI. Serum conditioning of AM requires synthesis of new protein(s); and the enzyme required for ROI production, NADPH oxidase, was only detectable in serum-conditioned cells. Moreover, serum-conditioned cells lost their ability to release ROI after transfer to serum-free medium, while cells maintained in serum-free medium acquired the capacity to release ROI after their transfer to serum-containing medium, demonstrating the reversibility of the phenomenon. Initial purification data indicate that conditioning is mediated by a discrete serum constituent, which precipitates 40-80% saturated ammonium sulfate, does not bind to Cibacron Blue columns, and has a molecular weight of 30,000 to 50,000, as determined by molecular exclusion chromatography. Unlike gamma interferon, which also enhances ROI release by macrophages, our serum-conditioning factor is not acid labile, retaining 67% of its activity after 120 min incubation at pH 2.0. Moreover, it does not appear to be a contaminating endotoxin, since LPS neither conditioned AM for ROI production, nor triggered ROI production by serum-conditioned AM. We propose that such a conditioning requirement may normally protect the lung against ROI-mediated tissue injury. However, during a pulmonary inflammatory reaction initiated by other mediator systems, the resulting transudation of plasma proteins into the alveolar spaces may condition AM in situ for ROI production.

Animals↗
PubMed1984

The effects of T-2 toxin on alveolar macrophage function in vitro.

T-2 toxin, a metabolite of several Fusarium species, is a mycotoxin of the trichothecene family which occurs in a variety of grains. Previous work in our laboratory showed that T-2 toxin is highly toxic to rat alveolar macrophages in vitro at submicromolar concentrations. The present investigation was undertaken to study the basis of the cytotoxic effects observed. The following parameters of macrophage function were measured: macromolecular synthesis, release of 51Cr, cellular ATP, phagocytosis, and alveolar macrophage "activation." The incorporation of radiolabeled leucine into acid-precipitable molecules was significantly inhibited within 1 hr of treatment at sublethal concentrations, although amino acid uptake was unaffected. Cell volume and release of 51Cr was unaffected by 0.1 microM T-2 toxin after 6 hr but evidence of significant leakage was seen after 18 hr treatment. The capacity of alveolar macrophages to phagocytize Saccharomyces cerevisiae and 3H-Staphylococcus aureus was significantly reduced whereas binding of 3H-S. aureus to the macrophage was not. Macrophage activation with endotoxin (Escherichia coli lipopolysaccharide) and mitogen-generated lymphokines, as monitored by incorporation of [14C]glucosamine, was significantly altered at 0.01 microM T-2 toxin. Thus, the data clearly demonstrate that T-2 is toxic to alveolar macrophage function in vitro and suggest that the primary mechanism of this toxicity is related to the inhibition of protein synthesis.

Adenosine Triphosphate↗