Improving hydrocarbon toxicity tolerance in poultry: role of genes and antioxidants.

Sustenance of smallholder poultry production as an alternative source of food security and income is imperative in communities exposed to hydrocarbon pollution. Exposure to hydrocarbon pollutants causes disruption of homeostasis, thereby compromising the genetic potential of the birds. Oxidative stress-mediated dysfunction of the cellular membrane is a contributing factor in the mechanism of hydrocarbon toxicity. Epidemiological studies show that tolerance to hydrocarbon exposure may be caused by the activation of genes that control disease defense pathways like aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2p45-related factor 2 (Nrf2). Disparity in the mechanism and level of tolerance to hydrocarbon fragments among species may exist and may result in variations in gene expression within individuals of the same species upon exposure. Genomic variability is critical for adaptation and serves as a survival mechanism in response to environmental pollutants. Understanding the interplay of diverse genetic mechanisms in relation to environmental influences is important for exploiting the differences in various genetic variants. Protection against pollutant-induced physiological responses using dietary antioxidants can mitigate homeostasis disruptions. Such intervention may initiate epigenetic modulation relevant to gene expression of hydrocarbon tolerance, enhancing productivity, and possibly future development of hydrocarbon-tolerant breeds.

Effects of burnt tire-ash on Na+/K+, Ca2+-ATPase, serum immunoglobulin and brain acetylcholinesterase activities in clarias gariepinus (Burchell, 1822).

Aquatic pollution may continue to deepen following the emergence of new class of toxicants. The present study investigated the effect of water-soluble fraction of burnt tire-ash on Clarias gariepinus. The fish were exposed to sublethal doses; 0.00 g/L, 2.24 g/L, 1.12 g/L and 0.56 g/L of tire-ash solution, representing 1/5, 1/10 and 1/20 of 11.2 g/L median lethal concentration (96 LC50), for 28 days, followed by 14 days recovery trial. Biological sampling was done on exposure day 1, 14 and 28, and on day14 recovery period for biochemical analysis such as the liver and gill Na+/K+ and Ca2+-ATPase, serum immunoglobulin (IgM) and brain acetylcholinesterase (AChE) of the experimental fish. Also, body biomass and behavior were evaluated. The behavioral responses exhibited by the fish to BTA exposure include reduced feeding, hypoactivity, air gulping and skin discoloration, which was observed to be concentration dependent. The body weight of 2.24 g/L and 1.12 g/L BTA-exposed fish decreased significantly than 0.56 g/L exposed fish and the control. Furthermore, findings revealed evident induction of Na+/K+ and Ca2 +-ATPase activities in both tissues, elevation of serum immunoglobulin content and inhibition of AChE activity in the brain of the exposed fish relative to the control. However, it was also observed that the biochemical parameters normalized after the recovery period. In conclusion, water-soluble fraction of burnt tire-ash produced toxicological effects in the experimental model, hence the present study provides the ecotoxicological insight of tire ash.

Tert-butylhydroquinone abrogates fructose-induced insulin resistance in rats via mitigation of oxidant stress, NFkB-mediated inflammation in the liver but not the skeletal muscle of high fructose drinking rats.

The effect of 21% fructose drinking water (FDW) (w/v) on some parameters of metabolic syndrome, hepatic, and skeletal muscular histology of rats was studied using standard techniques. Twenty male albino rats were divided into four groups of 5 rats each in this in vivo study. Group I received distilled water, group 2 received FDW, group 3 received FDW and metformin (300 mg/kg body weight daily, orally), group 4 received FDW and 1% tert-butylhydroquinone feed. FDW changed the serum leptin, triacylglycerol, very low-density lipoprotein, and C-reactive protein levels of the rats, inducing hypertriglyceridemia, oxidative stress, and inflammation in their liver (but not the skeletal muscle) and insulin resistance which were modulated with metformin and tBHQ as corroborated by liver and muscle histology. The study reveals the potentials of metformin and tBHQ in mitigating hepatic and skeletal muscular morphological changes arising from exposure to high fructose drinks. PRACTICAL APPLICATIONS: There has been an increase in the global consumption of fructose (either as a sweetner in beverages or soft and carbonated drinks) in the last few decades and this has been positively correlated with the global increase in metabolic complications. Regular intake of fructose contributes to the pathogenesis of lipid disorders, oxidant stress, and chronic inflammation, which are linked with the metabolic syndrome components (MetS) (obesity, insulin resistance, and cardiovascular diseases) as well as increased morbidity and mortality. Given that the approaches that have been applied to treat the MetS have not been able to totally arrest it, currenty study which showed that tBHQ abrogated fructose-induced insulin resistance, dyslipidemia, hepatic, and skeletal muscular pathology in the rats places tBHQ in the spotlight as a nutraceutical that could be of relevance in mitigating high dietary fructose-induced hepatic and skeletal muscular pathology.

Genotoxicity, oxidative stress and lysozyme induction in Clarias gariepinus chronically exposed to water-soluble fraction of burnt tire ash.

The safety of aquatic ecosystems has been compromised by numerous anthropogenic activities, especially leachates from non-point source toxicants, leaching into aquatic systems. This study evaluated the toxicity of the water-soluble fractions (WSFs) of burnt tire ash (BTA) on Clarias gariepinus via a battery of integrated biomarkers. Juvenile C. gariepinus were exposed to sublethal (0.56, 1.12, and 2.24 g/L) concentrations of BTA, derived from 11.2 g/L median lethal concentration (96 LC50), at duration intervals of 1, 14, and 28 days, followed by a recovery trial that lasted for 14 days. Serum biochemical parameters, antioxidant enzyme activities of the gill and liver, lysozymes activity and erythron profile were assessed. The findings of the present study revealed that BTA-WSF induced prominent alterations on biochemical parameters, lysozymes activity and antioxidant enzymes activities in the exposed fish. Furthermore, toxicant exposure promoted oxidative stress, cellular damage and genotoxicity (erythrocytic nuclear and cellular abnormalities) in the exposed fish. In general, a post-exposure trial showed partial recovery from the exposure effects of the toxicant, following the evident modifications of serum enzymes and erythron pathopathology in the experimental model. Biomonitoring of BTA, using sentinel aquatic species such as C. gariepinus, provides insights into the ecotoxicological potency of this toxicant.