METHODS: Search for related literature on salted fish,
smoking and alcohol consumption were performed via Science Direct, PubMed databases and Google Scholar. Articles
included in this study were from 2009 to 2017, with specific focus on salted fish, smoking and alcohol consumption
as risk factors of NPC. This study excluded all articles published prior to 2009 and articles involving other cancers.
Data were extracted independently by two different researchers and harmonized. Meta-analysis was conducted on the
obtained data, by using R package Meta to create funnel and forest plots.
RESULTS: The meta-analysis revealed that
salted fish, smoking and alcohol consumption were significantly associated to NPC risk with random effect model score
showing OR of 1.41 at 95% confidence interval (CI) of 1.13-1.75 (P<0.01), OR of 1.89 at 95 % CI of 1.49 - 2.38, and
OR: 1.42 at 95 % CI of 1.23 - 1.65 respectively. Our results also revealed significant association of salted meat, salted
vegetables, house type, wood dust exposure associated with NPC risk with p values less than 0.05.
CONCLUSION: This
study proposes that salted fish intake, smoking and alcohol consumption might be linked to NPC risk in Asians. Further
studies are necessary to ascertain the molecular mechanisms and clarify if the associated path that could function as
therapeutic target.
Objective: The current study was conducted to evaluate acute oral toxicity of LA on normal rats.
Methods: The study was conducted in accordance with the Organization for Economic Co-operation and Development guidelines (OECD 423) with slight modifications. LA was administered orally to female Sprague Dawley (SD) rats (n = 6/group) at a single dose of 300 and 2,000 mg/kg body weight, respectively, while normal control received vehicle only. Animals from all the three groups were monitored for any behavioural and toxicological changes and mortality for two weeks. Food and fluid consumption, body weight was monitored on daily basis. At the end (on day 15th) of the experimental period, blood was collected for haematological and biochemical analysis. Further, all the animals were euthanized, and internal organs were harvested for histopathological investigation using four different stainings; haematoxylin and eosin, Masson trichrome, Periodic Acid Schiff and Picro Sirius Red for gross pathology through microscopical observation.
Results: The study results showed no LA treatment-related mortality and morbidity at two different dosages. Daily food and water consumption, body weight, relative organ weight, haematological, and biochemical analysis were observed to be normal with no severe alterations to the internal tissues.
Conclusion: The current finding suggests that single oral administration of LA, even up to 2,000 mg/kg body weight, did not exhibit any signs of toxicity in SD rats; thus, it was safe to be used on disease models in animals.
METHOD: Cleistanthins A and B were isolated from the leaves of Cleistanthus collinus. Both the compounds were administered orally for 90 days at the concentration of 12.5, 25 and 50 mg/kg, and the effects on blood pressure, biochemical parameters and histology were assessed. The dose for sub-chronic toxicology was determined by fixed dose method according to OECD guidelines.
RESULT: Sub-chronic toxicity study of cleistanthins A and B spanning over 90 days at the dose levels of 12.5, 25 and 50 mg/kg (once daily, per oral) revealed a significant dose dependant toxic effect in lungs. The compounds did not have any effect on the growth of the rats. The food and water intake of the animals were also not affected by both cleistanthins A and B. Both the compounds did not have any significant effect on liver and renal markers. The histopathological analysis of both cleistanthins A and B showed dose dependent morphological changes in the brain, heart, lung, liver and kidney. When compared to cleistanthin A, cleistanthin B had more toxic effect in Wistar rats. Both the compounds have produced a dose dependent increase of corpora amylacea in brain and induced acute tubular necrosis in kidneys. In addition, cleistanthin B caused spotty necrosis of liver in higher doses.
CONCLUSION: The present study concludes that both cleistanthin A and cleistanthin B exert severe toxic effects on lungs, brain, liver, heart and kidneys. They do not cause any significant pathological change in the reproductive system; neither do they induce neurodegenerative changes in brain. When compared to cleistanthin A, cleistanthin B is more toxic in rats.