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H Babich

Publications and source records attributed to H Babich.

71 records · Page 4Linked to original sources

Dibromochloropropane (DBCP): a review.

A highly persistent, lipophilic, brominated organochlorine which is effectively used against nematodes, dibromochloropropane (DBCP) has been produced for agriculture since 1955. In 1975, production of DBCP in the United States reached 25 million lbs. However, investigations with laboratory animals, some of which were published in the early 1960s, have shown that DBCP decreases sperm mobility and spermatogenesis, disturbs the estrous cycle, reduces phagocytosis by white blood cells, and induces malignant tumors. Later studies with procaryotic and eucaryotic cells, including human sperm, have demonstrated DBCP to be mutagenic and to effect the genome adversely. In 1977 many of the employees at the Occidental Chemical plant in Lathrop, California, who had handled DBCP, were found to be either azoospermic or oligospermic. Subsequent surveys of employees handling DBCP at other chemical plants confirmed these findings. In 1977 on edible crops and in 1979 DBCP per se was detected in well waters. As a result of these studies, the Occupational Safety and Health Administration (OSHA) and the Environmental Protection Agency (EPA) in 1977 promulgated regulations restricting the use and handling of DBCP. In 1979, the EPA banned almost all agricultural uses of DBCP.

Animals↗

Abiotic factors affecting the toxicity of lead to fungi.

The toxicity of lead (Pb) to fungi in pure culture was influenced by several abiotic factors: pH, inorganic anions, clay minerals, and particulate (humic acid) and soluble organic matter. The toxicity of Pb was potentiated under acidic conditions (pH 5 and 6), and phosphate or carbonate anions reduced the toxicity, apparently as a result of the formation of sparingly soluble Pb salts. Clay minerals (montmorillonite greater than attapulgite greater than kaolinite) and particulate humic acid protected against the toxicity of Pb, presumably as the result of sorption, by cation exchange of the Pb to the exchange complexes, which reduced its availability for uptake by the fungi. Soluble organics, such as tryptone, yeast extract, cysteine, succinic acid, and increasing concentrations of neopeptone, also reduced the toxicity of Pb.

Aluminum Silicates↗

Differential toxicities of mercury to bacteria and bacteriophages in sea and in lake water.

Mixtures of anionic HgCl3-/HgCl4(2)-complexes were less toxic to terrestrial bacteria (Erwinia herbicola, Agrobacterium tumefaciens), to marine bacteria (Acinetobacter sp., Aeromonas sp.), and to bacteriophages (phi 11 M 15 of Staphylococcus aureus and P1 of Escherichia coli) than were equivalent concentrations of Hg as cationic Hg2+. The toxicity of 1 ppm Hg to A. tumefaciens. Aeromonas sp., and phi 11 M 15 was less in seawater than in lake water. Inasmuch as the Hg-Cl species are formed in environments of high chloride concentration, it was postulated that the lower toxicity of Hg in seawater was a result of the formation of HgCl3-/HgCl4(2)-complexes.

Acinetobacter↗

Toxicity of zinc to fungi, bacteria, and coliphages: influence of chloride ions.

A 10 mM concentration of Zn2+ decreased the survival of Escherichia coli; enhanced the survival of Bacillus cereus; did not significantly affect the survival of Pseudomonas aeruginosa, Norcardia corallina, and T1, T7, P1, and phi80 coliphages; completely inhibited mycelial growth of Rhizoctonia solani; and reduced mycelial growth of Fusarium solani, Cunninghamella echinulata, Aspergillus niger, and Trichoderma viride. The toxicity of zinc to the fungi, bacteria, and coliphages was unaffected, lessened, or increased by the addition of high concentrations of NaCl. The increased toxicity of zinc in the presence of high concentrations of NaCl was not a result of a synergistic interaction between Zn2+ and elevated osmotic pressures but of the formation of complex anionic ZnCl species that exerted greater toxicities than did cationic Zn2+. Conversely, the decrease in zinc toxicity with increasing concentrations of NaCl probably reflected the decrease in the levels of Zn2+ due to the formation of Zn-Cl species, which was less inhibitory to these microbes than was Zn2+. A. niger tolerated higher concentrations of zinc in the presence of NaCl at 37 than at 25 degrees C.

Bacteria↗

Sensitivity of Various Bacteria, Including Actinomycetes, and Fungi to Cadmium and the Influence of pH on Sensitivity.

A variety of microorganisms, including gram-negative and gram-positive eubacteria, actinomycetes, yeasts, and filamentous fungi, were tested for their sensitivity to cadmium (Cd). In general, the actinomycetes were more tolerant to Cd than were the eubacteria; gram-negative eubacteria were more tolerant to Cd than were gram-positive eubacteria. The period of exponential growth of the eubacteria and actinomycetes was extended in the presence of Cd. Wide extremes in sensitivity to Cd were noted among the fungi; there was no correlation between the class of fungus and tolerance to Cd. Fungal sporulation was more sensitive to Cd than was mycelial growth, as spore formation was inhibited at Cd concentrations that were noninhibitory to mycelial proliferation. The toxicity of Cd to the eubacteria, actinomycetes, and fungi appeared to be pH dependent, as toxicity was generally potentiated at pH 8 or 9.

Journal Article↗

Reductions in the toxicity of cadmium to microorganisms by clay minerals.

The clay minerals montmorillonite and kaolinite protected bacteria, including actinomycetes, and filamentous fungi from the inhibitory effects of cadmium (Cd). Montmorillonite provided greater protection than did equivalent concentrations of kaolinite. The protective ability of the clays was correlated with their cation exchange capacity (CEC). The greater the CEC, the greater the absorbancy of exogenous Cd by the exchange complex and the greater the protection. The greater protection afforded by montmorillonite, as compared to kaolinite, was correlated with its higher CEC. Clays homoionic to Cd did not protect against exogenous Cd, as the exchange complex was already saturated with Cd. Montmorillonite homoionic to Cd was more detrimental to microbial growth than was kaolinite homoionic to Cd, as more Cd was present on and apparently desorbed from the montmorillonite.

Journal Article↗

Effect of cadmium on fungi and on interactions between fungi and bacteria in soil: influence of clay minerals and pH.

Fungi (Rhizopus stolonifer, Trichoderma viride, Fusarium oxysporum f. sp. conglutinans, Cunninghamella echinulata, and several species of Aspergillus and Penicillium) tolerated higher concentrations of cadmium (Cd) when grown in soil than when grown on laboratory media, indicating that soil mitigated the toxic effects of Cd. In soil amended with clay minerals, montmorillonite provided partial or total protection against fungistatic effects of Cd, whereas additions of kaolinite provided little or no protection. Growth rates of Aspergillus niger were inhibited to a greater extent by 100 or 250 mug of Cd per g in soil adjusted to pH 7.2 than in the same soil at its natural pH of 5.1. However, there were no differences in the growth rates of Aspergillus fischeri with 100 or 250 mug of Cd per g in the same soil, whether at pH 5.1 or adjusted to pH 7.2. Growth of A. niger and A. fischeri in a soil contaminated with a low concentration of Cd (i.e., 28 mug/g), obtained from a site near a Japanese smelter, did not differ significantly from growth in a soil collected some distance away and containing 4 mug of Cd per g. Growth of A. niger in sterile soil amended with 100 mug of Cd per g and inoculated with Bacillus cereus or Agrobacterium tumefaciens was reduced to a greater extent than in the same soil containing 100 mug of Cd per g but no bacteria. The inhibitory effects of Agrobacterium radiobacter to A. niger were slightly reduced in the presence of 100 mug of Cd per g, whereas the inhibitory effects of Serratia marcescens were enhanced.

Antibiosis↗

In vitro cytotoxicities of 1,4-naphthoquinone and hydroxylated 1,4-naphthoquinones to replicating cells.

Using the human hepatoma cell line, HepG2, and the BALB/c mouse fibroblast cell line, 3T3, as the bioindicators in the neutral red cytotoxicity assay, the effect of hydroxyl substitution on the toxicity of 1,4-naphthoquinone was studied. The sequence of potency for the quinones was 5,8-dihydroxy-1,4-naphthoquinone > 5-hydroxy-1,4-naphthoquinone > 1,4-naphthoquinone >> 2-hydroxyl-1,4- naphthoquinone. Pretreatment of the cells with dicoumarol, an inhibitor of DT-diaphorase, enhanced the cytotoxicity of 1,4-naphthoquinone but not of the hydroxylated naphthoquinones. Pretreatment of the BALB/c cells with buthionine sulfoximine, an inhibitor of glutathione synthesis, enhanced the sensitivity of the cells to all the hydroxylated naphthoquinones but not to 1,4-naphthoquinone. A similar pretreatment of the HepG2 cells with buthionine sulfoximine enhanced the toxicity of the 2-hydroxy- and 5,8-dihydroxy-1,4-naphthoquinones but not of 5-hydroxy-1,4-naphthoquinone or of 1,4-naphthoquinone. Some differences were noted in the responses to the hydroxylated 1,4-naphthoquinones between buthionine sulfoximine-treated replicating cells and buthionine sulfoximine-treated isolated rat hepatocytes, a nonreplicating cell in culture. The use of a replicating cell system in studying the mechanisms of the cytotoxicity of quinones may be an important adjunct to studies using the isolated rat hepatocytes, which is the standard model system.

3T3 Cells↗

Progress and problems in evaluating and validating alternative assays in toxicology.

Various techniques have been proposed and subsequently developed as potential replacements for whole-animal topical toxicology assays. Comparisons of in vitro and in vivo endpoints, the solubility of test agents, solvent effects, interactions between components of complex test samples and the standardization of data presentation are factors that influence not only individual laboratory results but interlaboratory reproducibility and the acceptance of newly developed alternative methods. Representative alternative test systems for evaluating topical toxicity are discussed. Examples of problems, data and solutions based on the authors' experience and on experience in other laboratories are reviewed. Specific problems in choosing endpoints, comparing results, recognizing responses of different types of target cell, evaluating the influences of support media in culture and interpreting published animal-based data are included.

Animals↗

Indirect cytotoxicity of dental materials: a study with Transwell inserts and the neutral red uptake assay.

A modification of the Transwell insert methodology was evaluated by using the neutral red uptake (NRU) assay in a cytotoxicity test. The Transwell insert methodology was developed to assess the biocompatibility of solid materials used in dentistry and, when initially designed, used the release of radiochromium ((51)Cr) in the cytotoxicity assay. Another aim of this study was to evaluate different exposure regimes with which to assess cytotoxicity. The exposure regimes included: a 1-hour exposure in buffer followed by a 24-hour incubation in growth medium; a 2-hour exposure in buffer followed by a 24-hour incubation in growth medium; a 24-hour exposure in serum-limited medium; and a 24-hour exposure in a serum-sufficient medium. The bioindicator target was the Smulow-Glickman (S-G) human gingival cell line and the biomaterials were dental restoratives. The Transwell insert methodology with the NRU cytotoxicity assay as the cytotoxicity endpoint was effective in differentiating the potencies of the dental restoratives; a 2-hour exposure in buffer and a 24-hour exposure in serum-limited medium were the exposure regimes that most clearly differentiated the test agents according to their potencies. The sequence of cytotoxicity of the dental restoratives to the S-G cells was Vitremer > Ketac-Molar Aplicap > Flow-It.

Cell Death↗

Reproductive and carcinogenic health risks to hospital personnel from chemical exposure--a literature review.

Hospital personnel, both those involved directly (surgeons, anesthesiologists, operating room nurses) and indirectly (pharmacists, laboratory technicians) with promoting the well-being of patients, and those involved in maintaining the proper functioning of the hospital (housekeeping personnel, painters, machinists), may be exposed to chemicals that are potential reproductive and carcinogenic hazards. Waste anesthetic gases, sterilants, such as ethylene oxide and formaldehyde, antineoplastic drugs, methylmethacrylate, asbestos, and various organic reagents and solvents may induce genetic damage, cancer, congenital malformation, still-birth, and spontaneous abortion.

Anesthetics↗

Mediating role of metabolic activation in in vitro cytotoxicity assays.

Enzymatic activation of polycyclic aromatic hydrocarbons (PAHs) and its effect on cytotoxicity were studied using the neutral red viability assay as the end point. Benzo[a]pyrene was progressively cytotoxic to human hepatoma (HepG2) cells over a 1- to 3-d period, and after induction of monooxygenase activity with a polychlorobiphenyl (PCB) mixture (Arochlor 1254), cytotoxicity was increased about threefold. Concomitant with Arochlor exposure was an increase in the activity of 7-ethoxycoumarin odeethylase, which could be inhibited by exposure to alpha-naphthoflavone. Human keratinocytes (NHEK), but not fibroblasts (HFF), were sensitive to the cytotoxicity of benzo[a]pyrene. However, preexposure of the keratinocytes to Arochlor did not increase their sensitivity to benzo[a]pyrene. Neither the keratinocytes, fibroblasts, nor HepG2 cells were sensitive to acenaphthene. Addition of hamster or rat hepatic S9 mix, however, resulted in toxicity from benzo[a]pyrene and acenaphthene. 7,12-Dimethylbenz[a]anthracene was only mildly cytotoxic to the fibroblasts, and its cytotoxicity was not enhanced in the presence of rat or hamster S9 mix. Exposure of the HepG2 cells to 7,12-dimethylbenz[a]anthracene showed progressive toxicity over a 1- to 3-d period. Prior exposure of the HepG2 cells to Arochlor did not enhance their sensitivity to 7,12-dimethylbenz[a]anthracene. Human keratinocytes were sensitive to 7,12-dimethylbenz[a]anthracene, with cytotoxicity markedly increasing over a 1- to 3-d period.

9,10-Dimethyl-1,2-benzanthracene↗