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Human Health Risk Assessment of Perfluorinated Chemicals
Published in David M. Kempisty, Yun Xing, LeeAnn Racz, Perfluoroalkyl Substances in the Environment, 2018
Hepatocellular hypertrophy noted in these studies is often, but not always, accompanied by histopathological or biochemical evidence of peroxisomal proliferation and biochemical evidence of increased peroxisomal β-oxidation rates, commonly reported as increased cyanide-insensitive palmitoyl coenzyme A (CoA) oxidation rates in liver microsomal fractions. Increased liver weights and peroxisomal enzymes appear to be the critical effects for PFOA, occurring at serum levels as low as 14.1 μg PFOA/mL in mice (Wolf et al., 2008) and 70 μg PFOA/mL in rats (Perkins et al., 2004). The potency for induction of peroxisome proliferation increases with perfluorocarbon chain length and is proportional to the degree of hepatic accumulation of the compound (Kudo et al., 2006). PFOA and PFNA appear to be among the most potent peroxisome proliferator–activated receptor (PPAR)-α agonists (Wolf et al., 2012). PFDA may be the most potent peroxisomal enzyme inducer of the PFCAs, as a single injection of 50 mg/kg increased peroxisomal β-oxidation in the livers of male rats (Harrison et al., 1988). Peroxisomal enzyme induction may coexist with peroxisomal enzyme inhibition, such as the case with PFDA, PFDoDA, and PFOA (Singer et al., 1990; Borges et al., 1992). This increased peroxisomal β-oxidation is often accompanied by dose-related decreases in serum cholesterol, the ratio of high-density lipoprotein (HDL) to low-density lipoprotein (LDL), and triglycerides (Borges et al., 1992; Zhang et al., 2008; Minata et al., 2010; Bijland et al., 2011) after administration of PFCAs and PFSAs, with potency increasing with chain length. However, repeated-dose oral toxicity studies conducted with rats (Seacat et al., 2003) and monkeys (Seacat et al., 2002) with PFOS reported no signs of peroxisomal proliferation in the liver, even though hepatocellular hypertrophy and signs of liver toxicity, such as elevated serum liver enzymes and hepatocyte vacuolation, and decreased serum cholesterol were noted in both species. The reason for this discrepancy is unclear, as other studies conducted with PFOS in rats have reported clear induction of hepatocellular peroxisomal enzymes (Curran et al., 2008; Elcombe et al., 2012).
Evaluation of potential health effects associated with occupational and environmental exposure to styrene – an update
Published in Journal of Toxicology and Environmental Health, Part B, 2019
M.I. Banton, J.S. Bus, J.J. Collins, E. Delzell, H.-P. Gelbke, J.E. Kester, M.M. Moore, R. Waites, S.S. Sarang
It is not clear whether styrene, SO, some other styrene metabolite or some combination thereof is responsible for damaging the cochlea. Implication of a metabolite is suggested by the observation that co-exposure with ethanol (4 g/kg bw), an inducer of CYP2E1, both enhanced styrene metabolism and markedly potentiated its ototoxicity in rats (Loquet et al. 2000). This result is in striking contrast to that obtained in a similar experimental design with toluene, which is not capable of forming alkene-epoxide metabolites (Campo et al. 1998). Rats pretreated with the enzyme inducer phenobarbital exhibited enhanced metabolism of toluene and protection from ototoxicity, indicating that the parent compound is responsible for this effect (Pryor et al. 1991). Ethanol, a known competitive inhibitor of toluene metabolism (Sato, Nakajima, and Koyama 1981), slightly increased the ototoxicity of co-administered toluene, presumably due to the increase in circulating parent compound (Campo et al. 1998). Further support for a styrene metabolite’s role in cochlear damage is suggested by a study that found older rats (25–27 months of age) with presumed lower styrene metabolic capacity, were less sensitive to OHC loss and hearing threshold shift than young (3-month-old) rats exposed to 700 ppm for four consecutive weeks, with no evidence of recovery six weeks post-exposure (Campo et al. 2003). The older rats had heavier body weights (500 gm versus 300 gm for young rats) which could have impacted the findings of this study.
One-factor-at-a-time (OFAT) optimization of hemicellulases production from Fusarium moniliforme in submerged fermentation
Published in Energy Sources, Part A: Recovery, Utilization, and Environmental Effects, 2018
Zeinab H. Kheiralla, Nour Sh. El-Gendy, Hala A. Ahmed, Thanaa H. Shaltout, Mohamed M. D. Hussein
The fungal strain F. moniliforme expresses good xylanase activity, using the agro-industrial waste: corn cobs xylan as a carbon source and enzyme inducer (2,594.44 ± 62.25 U/l) in an SmF process. Upon optimization of the enzyme productivity by applying OFAT, the value approximately increased fourfold. The recorded maximum enzyme productivity of 10,950.11 ± 98.45 U/l was obtained under optimum SmF operating conditions of corn cobs xylan (6 g/l), yeast extract (4g/l), inorganic salts (1.5 g/l KH2PO4, 1.0 g/l MgSO4.7H2O, 0.2 g/l CaCl2, 0.4 g/l FeSO4.7H2O, and 0.3 g/l MnSO4.5H2O), initial pH (5), initial inoculum size (4%), 150 rpm, and temperature (30°C). Thus, optimization of process parameters is a prerequisite to enhance the enzyme yield and activity, which is very helpful in large-scale production. Further work is undertaken now for purification and characterization of the obtained xylanase and it will be published soon. However, upon application of the partially purified xylanase for saccharification of some agroindustrial wastes, tomato pomace, sugar beet pulp, and olive oil cake with hemicellulose content of 31.42, 38.77, and 34.35% (w/w), they yielded 800 ± 60, 1320 ± 87, and 210 ± 10 mg total reducing sugars/100 g substrate, respectively. That would add to its advantages for application in bioethanol production as it yielded a considerable amount of fermentable sugars.