Assessment of some tumorigenic risks associated with fresh and used cutting oil.
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Biomedical subjects
Publications and source records attributed to N K Mehrotra.
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In order to identify the tumour initiating constituent(s) of a mineral oil, jute batching oil (JBO), used in the processing of jute fibres, it was fractionally distilled in various boiling range fractions. The latter were then subjected to in vivo assessment of their aryl hydrocarbon hydroxylase (AHH) inducing potential in mouse epidermis. Fractions with almost similar AHH inducing potential were regrouped and studied for their tumour initiating potential over mouse skin following two-stage initiation-promotion protocol and using 12-O-tetradecanoyl phorbol-13-acetate (TPA) as tumour promoter. It was noticed that: (1) JBO as initiator, provoked local development of benign skin tumours over mouse back; (2) fractions of JBO boiling below 335 degrees C and above 399 degrees C accounted for most of the tumour initiating potential of the oil; (3) the histological features of the tumours (i.e. benign papillomas and keratoacanthomas) initiated by these fractions were similar to those developed after being initiated with unfractionated or reconstituted JBO; (4) removal of these fractions from JBO may be attempted which could decontaminate the batch oil from most of its tumorigenic components and make it safer for industrial use.
Single cutaneous application of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased epidermal oxidised glutathione reductase activity in adult mouse by almost 100%. Pretreatment of animals with vitamin A for a week resulted in 75% inhibition of TPA induced change in the enzyme activity which remained unaffected in skin treated with vitamin A alone. This biochemical change in skin induced by TPA and modulated by vitamin A has been discussed in relation to epidermal hyperplasia.
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Skin painting with 30 microliter of jute batching oil (JBO) for 8 days resulted in increased gross liver weight, microsomal protein content and benzo[alpha]pyrene hydroxylase activity of liver. Skin benzo[alpha]pyrene hydroxylase activity at the treated site increased by 10-fold. An investigation of cytochrome pigment status in liver and skin of treated animals showed a specific increase in P-448 level in both tissues. Single skin applications of JBO elevated the level of skin and liver benzo[alpha]pyrene hydroxylase activity to its maximum after 1 day and 2 days, respectively, which, in absence of further treatment with mineral oil, declined gradually to normal levels in due course. The results suggest that single or multiple cutaneous exposure(s) with JBO can increase carcinogen metabolising status of skin and liver which may be one of the causative factors for the tumorigenic effects of JBO in skin.
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To evaluate the carcinogenic activity of jute-batching oil (JBO), this substance was painted on the skin of ITRC mice up to 300 days. Initially hyper- and parakeratosis of the stratum corneum, acanthosis and spongiosis of the stratum Malpighii, hyperactivity of fibroblasts, and laying down of collagen fibres in the dermis were encountered at 100 days. This was followed by poor hair growth, acne formation and ulceration. As time passed, these animals partially adapted themselves to the oil-painting so that by 200 days hyperkeratosis and parakeratosis of the stratum corneum, as well as acanthosis and spongiosis of the stratum Malpighii, had almost disappeared. The ulcers healed and no more acne was visible; however, the baldness and loss of hair appendages persisted to 300 days. No carcinogenic changes in the skin or in the viscera of these mice were observed. On UV and IR spectroscopy no traces of any polycyclic aromatic hydrocarbons were found in the JBO sample. Mice, on the other hand, when painted with the known carcinogen 3,4 benzpyrene (BP), developed skin tumours, showing that the mice used in this study were not cancer-resistant. Also, when JBO was applied with BP, the time taken for tumour development in mice was shortened by about 4 weeks as compared to another group painted with the same dose of BP alone. This suggests a cancer-promoting activity which needs to be investigated further.
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The cirrhosis in male albino rats was produced after repeated subcutaneous injections of carbon tetrachloride, in dosage schedule as described. A fully developed cirrhosis was observed after 150 days. The silicosis in lungs was produced after single intratracheal injection of silica dust of particle size less than 5 microns and studied up to 180 days. The effect of damaged liver on the development of silicosis in the lungs was studied. It was found that pulmonary fibrosis caused by silica dust appeared to be a tissue reaction confined to the lung tissue alone. The dysfunction of liver did not exert any influence on fibrogenesis in the lungs.
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Several epidemics of febrile illnesses associated with haemorrhagic manifestations occurred in India during 1963 and 1964. These epidemics were restricted to the eastern coastal areas. However, in northern India, for the first time, a widespread epidemic of febrile illness associated with haemorrhagic manifestations occurred at Kanpur in 1968. In the present study, the virological findings of the epidemic are reported.The role of dengue type 4 virus in the epidemic is demonstrated by the isolation of the virus from a number of cases, including one with haematemesis, and conversion of antibody titres with dengue type 4 virus in the paired sera.
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